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UNITED STATES -OF AMERICA. 





























A GUIDE 



TO 



THE CLINICAL EXAMINATION 



OF 



THE URINE. 



FARRIXGTOX H. WHIPPLE, A.B. (Harv.). 









BOSTON: 

DAMRELL AND UPHAM, 

Ety (Bin (Corner Bookstore, 

283 Washington, corner School Street. 

1891. 



Y 



^ 



^V 



Copyright, 1891, 
By Farrington H. Whipple. 



John Wilson and Son, Cambridge. 



TO 

JSlg Kespecteti Instructor, 

EDWARD S. WOOD, A.M., M.D., 

this volume is dedicated 

By The Author. 



PREFACE. 



TT has been my aim in writing this little book 
merely to condense the essential features of 
larger and more diffuse works, and thus to pre- 
sent the subject in a more readily accessible and 
practical form. My hope is that the exposition 
has been as clear as is consistent with its brev- 
ity, and that the unavoidable repetition of many 
facts may serve to indicate their importance and 
facilitate their retention by the student. 

I am indebted for my facts to Dr. Wood of the 
Harvard Medical School, and also to the works 
of Roberts, Hoffmann and Ultzmann, Tyson, 
Birch-Hirschfeld, and Foster. 

To my friend and classmate, E. W. Taylor, 
thanks are due for his assistance with regard to 
the mechanical details connected with the prepa- 
ration of the work. 

F. H. W. 

Boston, Jan. 20, 1891. 



TABLE OF CONTENTS. 



Page 
INTRODUCTION 1 



CHAPTER I. Physical Characteristics of the Urine 7 

Consistency and Transparency 7 

Amount 9 

Specific Gravity 12 

Solids 15 

Color 16 

Odor 17 

Reaction 18 

CHAPTER II. Chemical Characteristics 22 

Normal Organic Constituents 23 

Urea 23 

Uric Acid 30 

Hippuric Acid 33 

Phenol . 34 

Coloring Matters. 

Urobilin (Urophasin) 35 

Uroxanthin (Indoxyl) 37 

Normal Inorganic Constituents. 

Chlorides 39 

Phosphates 43 

Sulphates 46 

Abnormal Constituents. 

Albumen . 47 

Sugar 56 

Leucine and Tyrosine 63 



Vlll TABLE OF CONTEXTS. 

Page 
Coloring Matters. 

Biliary 61 

Blood 06 

Accidental Constituents. 

Fat 72 

Chyle 73 

Fatty and Non-fatty Acids 74 

Ammonia Compounds and Alkalies 75 

Iodide of Potassium 70 

Extraneous Substances 76 

Metallic Salts 76 

Lead . 77 

Arsenic 71) 

Mercury 79 

CHAPTER III. The Sediment 81 

Fermentation of the Urine . . . 82 

Classification of Sediment 86 

Non-organized. 

Uric Acid and Urates 87 

Hippuric Acid 92 

Calcic Oxalate 92 

Phosphates 95 

Calcic Carbonate 97 

Cystine 98 

Xanthine 100 

Cholesterine 100 

Leucine and Tyrosine 101 

Bilirubin (Haematoidin) 103 

Organized. 

Mucus 103 

Leucocytes and Pus 105 

The Epithelium . ■ 108 

Blood 112 

Fibrin 113 

Renal Casts .114 

Fat 121 

Spermatozoa 121 



TABLE OF CONTENTS. ix 

Page 

Fungi 122 

Morbid Growths 125 

Entozoa 125 

Extraneous Matter 126 

CHAPTER IV. Urinary Concretions 127 

CHAPTER V. The Urine as affected by General 

Diseases 133 

CHAPTER VI. The Urine as affected by Local 

Diseases 144 

Disturbances confined to the Kidneys- .... 144 

Active Hyperemia ; 151 

Passive Hyperemia 153 

Acute Parenchymatous Nephritis ........ 155 

Chronic Parenchymatous Nephritis ...... 160 

Chronic Interstitial Nephritis 163 

Amyloid Degeneration 167 

Combined Renal Diseases 169 

Senile Atrophy 170 

Malignant Disease 171 

Abscess of Kidney 171 

Diseases of the Urinary Membranes below the 
Kidneys. 

Pyelitis 171 

Acute 172 

Chronic 173 

Ureteritis 173 

Cystitis 174 

Acute 175 

Chronic 176 

Inflammation of Neck of Bladder 177 

Prostatitis 177 

Urethritis „ . 178 

Blood in the Urine 178 

Pus in the Urine 179 



x TABLE OF CONTENTS. 

Page 
APPENDIX A. 

Method of Recording Urinary Examinations . . 181 

Differential Diagnosis 182 

Illustrative Cases . , 183 

APPENDIX B. 

Tabular Arrangement of the Characters of the 
Urine in the more Important Urinary Dis- 
eases 197 

APPENDIX C. 

Tabular Arrangement of Heller's Clinical Tests 200 



INDEX ................... 203 



A GUIDE 



CLINICAL EXAMINATION OF THE URINE. 



INTRODUCTION. 

THE processes of body metabolism are, on the 
one hand, constructive or anabolic, and on 
the other, destructive (retrograde) or katabolic. 
The products of the former, inasmuch as they are 
of service to the body in maintaining its vital 
functions are, in many instances, termed secre- 
tions, whereas the latter, inasmuch as they can no 
longer be of service to the living organism, and 
because the body strives to get rid of them, are 
called excretions. Speaking broadly, the excre- 
tions may be considered to be water, urea, carbon 
dioxide, and various organic and inorganic salts. 
Of these the lungs eliminate carbon dioxide and 
some water, the skin a considerable amount of 
water, some carbon dioxide, and an insignificant 
proportion of the salts, while the kidneys remove 
a very large amount of water, urea, its allied 

l 



2 CLINICAL EXAMINATION 

compounds, and most of the salts. Since these 
represent the final products of metabolism and 
under conditions of health are tolerably constant 
in appearance, composition, and amount, it would 
seem perfectly rational to examine them if it is 
desirable to know the probable condition of those 
vital processes of which the excreta are a product. 
Of the excreta, the urine offers greatest facilities 
for examination, and from it the most useful in- 
formation is obtained. 

The healthy urine, then, is a normal product of 
katabolism, depending for its continual production 
and in general unvarying composition, on the one 
hand, to the uninterrupted processes of tissue met- 
amorphosis, and, on the other, to a physiologi- 
cal and anatomical intactness of the kidney itself. 
The examination of the urine, therefore, not only 
shows the general condition of body metabolism 
(i. e. rapidity of the vital processes) and of the 
kidneys (i. e. their functional activity), but, in- 
asmuch as the urine passes, on its way out of the 
body, through a series of passages varying in 
structure and physiological function, it bears wit- 
ness to the condition of these as well. 

The most valuable information that the exami- 
nation of the urine gives is that which relates, in 
the first place, to the condition of the kidney and 
its capacity for work, and in the second, to the state 



OF THE URINE. 3 

of the channels by which the urine leaves the body. 
A knowledge of these facts is of great value, not 
only in interpreting disease, but also in furnish- 
ing grounds upon which to base a prognosis and 
the proper plan of treatment. 

Before passing to the consideration of the urine 
itself, it may be well to review briefly the nature 
of the process by which the kidney performs its 
work. 

In the first place there is the theory of Bowman, 
in which the separation of the urine is regarded as 
partly one of filtration and partly one of elaboration. 
Certainly the long and tortuous tubuli uriniferi, 
with their wealth of epithelium and intimate rela- 
tion to the capillary loops, suggest the probability 
of epithelial elaboration, while the Malpighian cor- 
puscle, with its thin and insignificant layer of epi- 
thelium enveloping the tortuous knot of capillaries 
and the immediate connection of the latter with 
the renal artery where the pressure is tolerably 
high, suggests separation under pressure, i. e. 
a kind of filtration. 

In the second place there is the theory of Lud- 
wig. According to his view, the separation is one 
of simple osmosis. The blood, drained, in the 
glomeruli, of much of its water, passes in a thick- 
ened state to the capillaries surrounding the con- 
voluted tubes. Here the conditions for osmosis 



4 CLINICAL EXAMINATION 

are perfect, — two fluids of different densities on 
either side of an animal membrane ; the thin 
watery fluid that has descended from the Malpigh- 
ian bodies is in the tubes, while the thickened 
blood, separated from the former by the capillary 
wall, the basement membrane and its epithelium, 
circulates in the capillaries. Thus there is an 
interchange of fluids, the result of which is the 
elaborated urine. The original objection to this 
theory, that an acid fluid is obtained by osmosis 
from an alkaline one, no longer holds, since labo- 
ratory experiment shows that such may actually 
take place. 1 On the other hand, if the tubules 
are stripped of their epithelium, as they often are 
in disease, urea is no longer eliminated so abun- 
dantly, although the conditions for osmosis remain 
even better than before. 

In view of all the facts, the theory of Ludwig 
must be set aside and some such view as Bowman's 
adopted. But even here the " filtration " must be 
of a peculiar sort, and not wholly dependent on 
pressure; neither is it diffusion, but it probably 
partakes somewhat of the nature of an active pro- 
cess. 2 However this may be, under normal condi- 
tions the water and more diffusible salts, and 

1 Vide Tyson, Practical Examination of the Urine, 6th ed., 
p. 14. 

2 Vide Foster, Textbook of Physiology, 5th ed., p. 656 etseq. 



OF THE URINE. 5 

under abnormal conditions such substances as al- 
bumen, sugar, and haemoglobin, pass out through 
the glomeruli. Again, the epithelium has a two- 
fold activity, for it not only secretes some of 
the urinary constituents, e. g. hippuric acid and 
acid sodium phosphate, but it also has a se- 
lective function, — picking out of the blood, as it 
were, the products of retrograde metamorphosis, 
viz. urea and biliary pigments. There is also 
reason to believe that the epithelium shares in the 
production of water. 

The separation of the urine is therefore a com- 
plex process, and no one theory can satisfactorily 
explain all the facts. 

In the following pages frequent use will be made 
of the terms relative and absolute amount; they 
therefore require explanation at the outset. By 
the term u absolute amount " is meant the quantity 
that is actually excreted in twenty-four hours. 
It is generally used with reference to the solid 
constituents; but in performing the ordinary 
clinical tests, the amount of the solids will ap- 
parently vary according as they are dissolved in 
much or little water. This apparent proportion 
between the solids and the water is spoken of as 
the "relative amount." 



CHAPTER I. 

PHYSICAL CHARACTERISTICS OF THE URINE. 

Consistency and Transparency. — Xormal urine, 
when freshly passed, is a clear limpid fluid, drop- 
ping and flowing readily, like water. 

Shortly after standing, there appears, some- 
where between the top and bottom, a faint cloud 
made up of mucus and exfoliated epithelium de- 
rived from the genitourinary tract. On longer 
standing, fermentative processes begin, the result 
of which is to render the urine, by the deposi- 
tion of a sediment, more or less cloudy. The 
exact nature of this process will be considered 
further on. 

The urine when freshly passed may be cloudy, 
especially if it be neutral or slightly alkaline, 
as, for instance, after a meal composed largely of 
vegetables or milk. This is owing to the sepa- 
ration of earthy phosphates ; they gradually settle 
to the bottom, forming a somewhat bulky sedi- 
ment. The addition of a few drops of acid will 
cause their immediate disappearance. 



8 CLINICAL EXAMINATION 

A temporary cloudiness is of no account; but 
if the urine is habitually turbid when passed, it 
indicates trouble. A transparent urine, however, 
is not necessarily normal. 

Again, the urine may be perfectly clear when 
passed ; but as its temperature falls, a deposit of 
mixed urates (K, Na, Ca, Mg) is not unlikely to 
occur. These salts, although soluble at the body 
temperature, are promptly precipitated in the cold, 
giving rise to a pinkish or reddish deposit char- 
acterized as " lateritious, " or " brick-dust, " The 
application of heat will cause the deposit, if it be of 
urates, to disappear ; if of phosphates, to increase. 

The urine of saccharine diabetes, although per- 
fectly clear when passed, becomes turbid in a very 
short time. This is due to the growth of the sugar 
spore. In addition, a film covers the surface. 

In tropical climates the urine is often cloudy, if 
not indeed decidedly milky, due to the presence of 
chyle. Ordinarily, sediments, on standing, settle 
to the bottom, leaving a clear supernatant fluid. 
Such is not the case with chylous urine : the 
cloudiness remains diffused through the fluid for 
many hours. 

Finally, if the urine is alkaline, and contains 
pus, it may be viscid or "ropy." 

If urine be shaken, a slight foam is developed 
on the surface, but it quickly disappears when 



OF THE URINE. 9 

quiet is restored. It is said to be more permanent 
if the urine contain sugar or albumen. If the 
urine contain bile pigment, a permanent foam is 
developed, which is yellow or yellowish green in 
color. 

Amount. — Speaking broadly, the amount of 
urine passed may be taken as an index of the renal 
activity. On the average, the quantity for the twen- 
ty-four hours may be considered as not far from 
1500 c. c. (40 to 50 oz. ). This is, however, subject 
to considerable variation, not only between differ- 
ent individuals, but also in the same individual 
at different times. This variation depends on 
many conditions, viz. : — 

a. There is a diurnal variation that is inde- 
pendent of other influences, — most being passed 
in the afternoon, less in the forenoon, and least 
during the night and early morning. 

b. Drink and Food. — An excess of fluid taken 
into the system will cause a temporary increase in 
the flow of urine. Thus, a separation of 838 c. c. 
in an hour has been observed to follow the drink- 
ing of an excessive amount of water on an empty 
stomach. The ingestion of food has an influence 
upon the flow, for after meals there is an increase, 
whereas fasting will cause a diminution. 

c. Exercise. — Prolonged exercise causes an in- 
creased activity of the sweat glands ; and, bearing 



10 CLINICAL EXAMINATION . 

in mind the complementary action between these 
glands and the kidneys, it follows that at the same 
time with the increased sweat production the flow 
of urine will be diminished. For the same reason, 
external cold, by decreasing the activity of the 
sweat glands, results in an increased flow of urine. 
Similarly, the reverse is true of external warmth. 
Hence it is that during the winter the flow of urine 
is on the average greater than it is in summer. 
All this indicates that a part of the renal function 
is concerned in preserving a normal aqueousness 
of the blood. 

cl. Vaso-motor Action. — Nerve filaments are dis- 
tributed to the blood-vessels of the kidney. By 
disturbances in their function the flow may be in- 
creased, as in spastic polyuria, or diminished, as 
in suppression following a "catheter chill." Such 
disturbances are, in general, only temporary. 

e. Finally, a diminished flow may be the result 
of mechanical obstruction somewhere in the urinary 
passages. 

Pathologically, the amount varies a great deal. 
Certain diseases are characterized by a constant 
variation from the normal. In some, the flow is 
increased for a time, followed by a decrease; in 
others, the decrease is permanent from the be- 
ginning. In all cases of Bright's disease, there is 
a decided diminution at the close of life. 



OF THE URINE. 11 

In acute stages of disease the amount is dimin- 
ished. At the same time, the color as well as the 
specific gravity is high. As the acute stage passes 
over into the convalescent, the amount begins to 
increase, and even exceeds the normal, - — more so 
in acute nephritis than in ordinary acute disease ; 
but as convalescence becomes established, it falls to 
normal. In this way the turning or critical point 
may be approximately determined. Intermittent 
fever is, however, an exception, for the febrile 
character of the urine appears only on the day 
after the chill. 

The amount is of greater importance in chronic 
than in acute disease. 

In both forms of diabetes (mellitus and insipi- 
dus) the amount is greatly increased; viz. 3 to 6 
litres in 24 hours. In chronic interstitial nephri- 
tis and amyloid degeneration of the kidney, the 
amount is increased; viz. 4 to 6 litres in 24 
hours. 

In chronic affections, combined with dropsy, the 
urine is much diminished, since the excess of water 
in the blood forms a constituent of the effusion. 
If absorption from the cellular tissues and serous 
cavities takes place, th£ amount of urine returns 
to the normal. 

According to the amount of urine passed, three 
terms are employed, viz. : Polyuria, if the flow is 



12 CLINICAL EXAMINATION 

increased above the normal; Oliguria, if it be 
much less than normal; Anuria, or suppression, 
if no urine is passed. Each is to be regarded as 
a symptom, and not a disease. 

Anuria, or suppression, may be due to either 
of two general classes of causes, a. Organic dis- 
ease of the kidney or disturbances of innervation. 
b. Mechanical obstruction of any sort in the course 
of the excretory channels. Hence the former may 
be regarded as non-obstructive and the latter as ob- 
structive suppression. These two classes vary in 
their course and symptoms. They will be again 
reverted to. 

Specific Gravity (sp. gr. ). — In health the spe- 
cific gravity varies within tolerably wide limits. 
Inasmuch as it is a measure of the concentration 
of the urine, it will be influenced by all those con- 
ditions that alter the relation of the water to the 
solids; namely, drink, exercise, perspiration, the 
season (summer, winter), and nervous disturb- 
ances. The usual range of density, in health, may 
be put down as from 1018 to 1024, or, on the av- 
erage, for mixed 24 hour urine, 1021. Pathologi- 
cally, the variation is between 1003 and 1050. 

In the acute febrile stat^, the amount of urine is 
diminished, while the urea, uric acid, and sul- 
phates are absolutely increased. Consequently, in 
such cases the specific gravity ranges high. In 



OF THE URINE. 13 

acute disease the appetite is greatly reduced, so that 
the increase of solids in the urine is probably at 
the expense of the permanent tissues; hence the 
wasting and emaciation of disease. As convales- 
cence supervenes, the amount of urine increases 
beyond the normal, while the specific gravity falls 
below. 

In chronic diseases, the total solids as well as the 
specific gravity fall below the normal. In general, 
chronic disease may be suspected when the amount, 
specific gravity, and total solids are just below 
normal. The two forms of diabetes are an ex- 
ception. In both cases the total solids are largely 
in excess (125 to 150 grams), as well as the water; 
but in diabetes mellitus the sp. gr. is high, on ac- 
count of the presence of a large amount of sugar, 
while in diabetes insipidus the sp. gr. is low, be- 
cause the water is relatively increased. Hyclruria 
resembles diabetes insipidus. The water is in- 
creased and the sp. gr. is low, but in hydruria the 
total solids are quite normal, or only slightly di- 
minished. In chronic interstitial nephritis and 
amyloid degeneration the amount of water is large, 
but the sp. gr. is low, because the solids are di- 
minished. 

In general, during convalescence the specific 
gravity is below normal, the amount of water in- 
creased; while the solids are about normal. 



14 CLINICAL EXAMINATION 

In chronic parenchymatous nephritis and pas- 
sive congestion, the amount of fluid is diminished, 
as well as the total solids, yet the specific gravity 
is high. 

In a general way, the following deductions may 
be made : — 

If the urine be diminished and the specific grav- 
ity high, it indicates, in health, either that little 
water has been ingested, or that free perspiration 
has taken place. Pathologically, it indicates the 
active stage of an acute or an exceptional chronic 
disease. 

If the amount be large, and the specific grav- 
ity low, it indicates, in health, that excessive 
drinking has occurred. Pathologically, it sug- 
gests hydruria, diabetes insipidus, chronic in- 
terstitial nephritis, amyloid degeneration, and 
recovery from acute disease. 

If the quantity as well as the specific gravity 
be low, it indicates a serious condition, which 
usually obtains just before death, and, in con- 
nection with kidney disease, betokens the dan- 
gers of uraemia. In some instances it indicates 
suppression, either obstructive or non-obstructive. 

The specific gravity is most conveniently taken 
by means of the urinometer, various patterns of 
which, including the urinometer glass, are offered 
for sale. In general, those that have the olive- 



OF THE URINE. 15 

shaped bulb or float, and read from 1000 to 1060, 
will be found most convenient for all practical 
purposes. 

If, in determining the specific gravity the quan- 
tity of urine be too little to fill the urinometer 
glass, it may be diluted with distilled water suffi- 
ciently to fill the glass to the required height. 
From the specific gravity of this mixture that of 
the urine can be calculated. E. g. suppose that 
four volumes of water are added to one of urine, 
making five volumes in all, and that the specific 
gravity of the mixture is 1004, then that of the 
urine will be 1000 -f (4 X 5) = 1020. In such 
calculations the reading of the urinometer must 
be as accurate as possible, lest the error of 
reading be also multiplied by the number of 
volumes. 

Solids. — Under normal conditions the total sol- 
ids amount to about 72 grams in 24 hours. As a 
rule, females eliminate less and children more per 
kilogram of weight than males.^ 

An estimation of the total solids is of great 
value, inasmuch as they indicate (a) the rapidity 
of the vital processes, and (b) the capacity of 
the kidney for work. To make such knowledge 
of value, it is important to know the amount of 
urine passed, and also at what time or during 
what periods of time it is passed. 



16 CLINICAL EXAMINATION 

The solids may be roughly estimated from the 
specific gravity by multiplying the last two figures 
by 2J for each litre of urine. E. g. quantity of 
urine passed in 24 hours, 1500 c. c. ; sp. gr. 1021. 
Then 21 X 21 = 49 for 1 litre, or 1000 c.c. ; for 
1500 c.c, or 1^ litres, 49 X 1|- = 73|, which rep- 
resents the amount in grams of the total solids 
in the above specimen. 

Color. — The color of urine in health is a light 
yellow or amber, but varies in intensity from the 
palest straw to a full amber or red. A dark urine 
is abnormal. 

The most usual variations of color are due either 
to dilution, i. e. anything that causes a relative 
increase in the water ; or to concentration, i. e. 
any cause for a relative decrease of the water. 
Such causes have been studied in the preced- 
ing paragraphs. In fever there is an actual in- 
crease of metabolic processes, and consequently an 
absolute increase of color pigment. Hence fever 
urines are high-colored. Some maintain that the 
peculiar high color of fever urines is due to an 
abnormal pigment, uroerythrine. 

It is therefore common to classify the color of 
urine as pale, normal, high, or dark, 

A dark color always means the presence of an 
abnormal coloring matter. Usually it is some 
shade of brown or gTeen. and in most cases is due 



OF THE URINE. 17 

to blood or bile. Bile pigment may give rise to 
either a brown or green hue. If the color be clue 
to bile, on shaking the urine in a test tube a per- 
manent greenish-yellow foam is developed. 

Rarely, the color may be a dirty blue. In such 
instances, there is a similarly colored sediment, 
and upon the surface a dark blue film. The urine 
is usually alkaline, and chiefly found associated 
with cholera and typhus fever. The pigmentation 
is due to indigo, through the decomposition of 
indoxyl. 

Finally, the color may be influenced through the 
absorption by the system of various substances. 
E. g. creosote, tar ointment, carbolic, gallic, and 
salicylic acids may give rise to dark urines. Rhu- 
barb and santonin impart a yellow shade to the 
acid urine, which on the addition of an alkali 
turns to red. Senna communicates a brownish, 
and logwood a reddish tinge to the urine. 

Odor. — In general, the odor is characteristic, 
and is spoken of as " urinous. " It is of no conse- 
quence unless ammoniacal. Certain drugs (tur- 
pentine, copaiba, cubebs, oil of sandal-wood) and 
certain articles of food (asparagus, garlic) com- 
municate peculiar and characteristic odors to the 
urine. Diabetic urine, when fresh, has an odor of 
new-mown hay. Turpentine imparts to the urine 

the odor of violets. 

2 



18 CLINICAL EXAMINATION 

Reaction. — The reaction of the mixed twenty- 
four hour urine is always acid, and is equivalent 
to from 2 to 4. grams of oxalic acid. The acid- 
ity is probably due to the acid sodium phosphate 
(NaH 2 P0 4 ), assisted perhaps by other acid con- 
stituents, such as uric and hippuric acids, and, 
under some circumstances, by a few of the fatty 
acids, e. g. acetic and lactic. 

Phosphoric acid is tribasic (H 3 P0 4 ), and hy- 
drogen can be replaced by either one, two, or 
three equivalents of sodium; namely, Na t oP0 4 , al- 
kaline ; Na 2 HP0 4 , neutral, or slightly alkaline ; 
NaH 2 P0 4 , acid. The neutral phosphate, Na 2 HP0 4 , 
is a constituent of the blood. The dibasic uric 
acid (H 2 U) is also present in the blood, and be- 
tween them a mutual exchange of H for Na 
occurs, viz. : — 

Na 2 HP0 4 + H 2 tJ == NaHU + NaH 2 P0 4 . 

The acid sodium phosphate passes by osmosis 
through animal membranes, whereas the neutral 
salt does not. Hence it is that the kidneys sepa- 
rate the former, and not the latter. 

The acidity of the urine may be neutralized by 
any compound of ammonium, such as urea. By 
organic decomposition, urea takes up one mole- 
cule of water, giving two molecules of ammonia, 
and one molecule of C0 2 . These readily recom- 



OF THE URINE. 19 

bine with one more molecule of water to form 

one molecule of amnionic carbon- •; 

ate, (NH 4 ) 2 C0 3 . This reaction /&....?.!. 



NH„ HH 



goes on in all urines on standing, 

and it may be hastened in the 

fresh by the addition of a little stale urine, as that 

of an old cystitis. 

Pasteur showed that urea was changed into 
carbonate of ammonium by the action of a mi- 
crococcus (M. Urese), and it is now pretty well 
established that the production of ammoniacal 
urine is a kind of bacterial fermentation. The 
fact that stale urine hastens the change is ex- 
plained on the ground that it is highly charged 
with bacteria of all kinds, including the M. 
Ureae. 

Another view of the alkaline fermentation is 
based on the destructibility of urea by a peculiar 
ferment discovered by Musculus ; he recommends 
a paper saturated with this ferment as a very sen- 
sitive test-paper for urea. The alkaline urine of 
cystitis is filtered ; the filter-paper is washed with 
distilled water until it no longer has an alkaline 
reaction. It is then dried and colored with tur- 
meric. Urea itself does not react on turmeric, but 
the urea is decomposed to ammonium carbonate by 
the absorbed ferment, and the paper is therefore 
colored brown. 



20 CLINICAL EXAMINATION 

If the urine is ammoniacal when passed, it nearly 
always indicates a cystitis or pyelo-cystitis. 

The alkalinity, however, may be due to a fixed 
alkali (Na or K) circulating in the blood. In case 
of doubt the vapor of the heated urine may be 
tested with turmeric paper. If the test responds 
the alkali must be volatile (NH 4 ). 

When the blood is excessively alkaline, as after 
a meal composed largely of vegetables or milk, it 
modifies the acidity of the urine, and in fact may 
for a short time render it slightly alkaline. 

Urine may be excessively acid from concentra- 
tion, as is the case in fevers. 

A highly acid urine favors the deposition of ox- 
alate of calcium and uric acid crystals. If separa- 
tion occurs within the urinary passages, a local 
irritation is set up, which may lead to more or 
less serious inflammation, as well as to the for- 
mation of calculi. 

After standing awhile at a moderate tempera- 
ture, the acidity of the urine increases ; the color 
becomes high, and the normal mucous cloud, in- 
creased by the separation of the acid urates and 
uric acid, finally settles to the bottom. This is 
called the stage of acid fermentation. After 
longer standing, though quite rapidly in hot 
weather, the reaction changes to alkaline, the 
color becomes paler, and, owing to the deposition 



OF THE URINE. 21 

of many substances to be studied hereafter, the 
turbidity increases. This change constitutes the 
stage of alkaline fermentation. 

Fresh urine, hermetically sealed in an aseptic 
vessel, will remain fresh for years. 



22 



CLINICAL EXAMLNATION 



CHAPTER II. 



CHEMICAL CHARACTERISTICS. 



The constituents of the urine are numerous, 
and, although subject to wide variations, even in 
health, vet the following table may be taken as 
showing the average amounts eliminated in the 
twenty-four hours. 

Urinary Constituents passed in Twenty-pour Hours. 
(After Parkes.) 

By an average 

mass of 66 kilos Per 1 kilo of 
(145 lbs.). body weight. 

Grams. 

Water 1500.000 23.0000 

Total solids 72.000 1.1000 

Urea 33.180 .5000 

Uric acid 0.555 .0081 

Hippuric acid 0.400 .0060 

Kreatiniii ........ 0.910 .0140 

Pigment and other substances . 10 000 .1510 

Sulphuric acid 2.012 .0305 

Phosphoric acid 3.164 .0480 

Chlorine 7.000 .1260 

(8.21) 

Ammonia 0.770 

Potassium ....... 2.500 

Sodium 11.090 

Calcium 0.260 

Magnesium ....... 0.207 



OF THE URINE. 23 

It will be seen that urea and chlorides are the 
principal constituents, and, the others remaining 
unchanged, any marked increase or decrease in 
the excretion especially of urea or of chlorides will 
notably influence the specific gravity of the urine. 
The same is true to a lesser degree of the other 
solids. 

Normal Organic Constituents. 

Urea (U) is the most important solid constitu- 
ent of the urine. It is the final product of the 
retrograde (oxidative) metamorphoses of the ni- 
trogenous tissues. As such, it is formed through- 
out the body and taken up by the circulating blood, 
from which it is separated by the functional ac- 
tivity of the kidneys. When for any reason the 
kidneys become incapable of eliminating urea, the 
sweat glands to a certain extent assume their lost 
or impaired function, and urea is then detected in 
the sweat. 

Urea, however, is not formed from the albu- 
minoid tissues direct, but it has been found that 
many intermediate stages, with their correspond- 
ing products, exist. Among the latter are uric 
acid, leucine, and tyrosine. When, for exam- 
ple, the oxidative processes are seriously impaired 
(e. g. acute yellow atrophy of the liver and typhus 
fever), no urea is found in the urine, but in its 



2 i CLINICAL EXAMINATION 

place leucine and tyrosine ; furthermore, if these 
substances are ingested by a healthy individual, 
his nitrogenous excreta (U) is found to be in- 
creased by just so much nitrogen as was contained 
in the amount of leucine and tyrosine taken into 
the system. 

The average amount of urea passed in twenty- 
four hours is from thirty to forty grams, with a 
normal variation of one fifth below or above this 
amount. Women and children excrete less urea 
than men, but children more, in proportion to 
their body weight. A normal urine may be said 
to contain 2-|% of urea. 

Urea can be made artificially in many ways, and 
most readily from ammonium cyanate. It is a 
white (somewhat brownish when made from urine) 
crystalline solid, freely soluble in water and al- 
cohol, but insoluble in ether. By the addition of 
nitric acid, nitrate of urea is formed. Under 
the microscope the nitrate crystals appear singly, 
or in overlapping layers, as rhombic or hexagonal 
plates. 

Tests for Urea. — The clinical method of testing 
for urea is to add a drop or two of nitric acid to a 
like quantity of urine in a watch crystal. If the 
amount of urea present is normal, in from twenty 
to thirty minutes delicate crystals of nitrate of 
urea appear in the fluid. A very warm room or 



OF THE URINE. 25 

an excess of urea will hasten the crystallization, 
and vice versa. This is only an approximate test, 
and if the acid is impure (contains HN0 2 ) it de- 
composes the urea, thus : 

CH 4 N 2 + HN0 8 + HN0 2 = NH 4 N0 8 + H 2 -f C0 2 + N 2 . 

The mixture should never be warmed, as it facil- 
itates the decomposition. In cases where the urea 
has already decomposed (cystitis), this test can- 
not of course be applied. 

As it is often of importance to know the precise 
quantity of urea excreted, many quantitative tests 
have been devised ; but of these the following, based 
on the fact that a chlorinated compound acting 
upon urea gives rise to a single gas, is the most 
popular, viz. : 

CH 4 N 2 + 3 NaOCl = 3 NaCl -f 2 H 2 + C0 2 -f N 2 . 

The same reaction occurs with either calcic 
hypochlorite or sodic hypobromite. 

The apparatus for performing the test consists 
essentially of two parts. 1. A burette graduated 
to 60 c.c, as indicated in the figure. 2. A double- 
bulbed flask, each bulb of 100 c.c. capacity, and 
united as indicated in the figure. The burette, 
fastened by a clamp to a retort stand, is immersed 
in a large beaker of water, so that the fluid in- 
side of the burette stands at the zero line ; or the 



26 



CLINICAL EXAMLNATLON 



burette may be similarly, but tightly, adjusted to 
a perforation in a cork which fits the mouth of the 




Fig. 1. Apparatus for the 
Quantitative Estimation of 
Urea. 



beaker. A few perforations of the cork outside the 
burette are necessary in order that air may escape 
from the beaker when the apparatus is put in oper- 
ation. The flask, with a tightly fitting cork through 
which a bit of glass tube is passed, is then con- 
nected with the burette by rubber tubing. 

To perform the test, 5 c.c. (2*- c.c. if high col- 
ored and concentrated) of urine are poured into 
one of the bulbs, while a sufficient amount of calcic 
hypochlorite is placed in the other. Having con- 



OF THE URINE. 21 

nected the two parts of the apparatus as indicated 
in the figure, the double-bulbed flask is so agi- 
tated as to allow thorough commingling of the 
urine with the hypochlorite. Effervescence at 
once commences, and the liberated nitrogen gas 
passes over into the burette and drives out the 
fluid. When effervescence has ceased the amount 
of water displaced by the gas is read off, and from 
that the quantity of urea is calculated, — based 
on the fact that at 0° C. and 760 mm. barometer, 
1 gram urea = 370 c. c. N. For example : if, when 
the reaction has run to an end, 40 c. c. of nitrogen 
are recorded on the burette, in accordance with 
the assumption that 1 gram of urea = 370 c. c. N, 
the following proportion can be made : 

370 : 40 = 1 : x (= .1084-). 

This represents the amount of urea (in grams) in 
5 c.c. of urine (the quantity used in the experi- 
ment). Obviously, in 1500 c.c. urine (assuming 
that to be the amount passed in 24 hours) there 
must be (.108 x ■Uyw _.) 32.4 grams. 

In all tests for urea, save the above, albumen 
must first be removed. 

To avoid the necessity of calculation, the follow- 
ing table has been arranged, from which at a glance, 
the cubic centimeters of nitrogen having been de- 
termined, the amount of urea can be estimated. 



28 



CLINICAL EXAMINATION 



TABLE FOR UREA IN URINE. 





For 15-20° 


C. 63-69° Fabr. Us 


ing 5 c. c. 


Urine. 


. c. 

rogen 


Urea per 

Litre 
in Grams. 


Urea per 

Ounce 

in Grains. 


c. c 

Nitrogen. 


Urea per 

Litre 
in Grams. 


Urea per 

Ounce 

in Grains 


20 


1024 


4.75 


36 


18.44 


8.86 




10.50 


5.06 




18.70 


9.00 


21 


30.76 


5.15 


37 


18.96 


9.09 




11.01 


5.30 




19.21 


9.25 


22 


11.27 


5.39 


38 


19.47 


9.34 




11.52 


5.54 




19.73 


9.48 


23 


11.78 


5.62 


39 


19.98 


9.58 




12.04 


5.78 




20.24 


9.73 


24 


12.29 


5.87 


40 


20.49 


9.82 




12.50 


6.01 




20.75 


9.96 


25 


12.81 


6.17 


41 


21.00 


10.12 




13.06 


6.26 




21.26 


10.21 


26 


13.32 


6.40 


42 


21.52 


10.35 




13.58 


6.49 




21.77 


10.44 


27 


13.83 


6.65 


43 


22.03 


10.60 




14.09 


6.74 




22.28 


10.69 


28 


14.35 


6.88 


44 


22.54 


10.83 




14.60 


7.03 




22.80 


10.99 


29 


14.86 


7.13 


45 


23.05 


11.08 




15.11 


7.27 




23.31 


11.23 


30 


15.36 


7.36 


46 


23.57 


11.31 




15.62 


7.51 




23.82 


11.47 


31 


15.87 


7.61 


47 


24.08 


11.56 




16.13 


7.75 




24.34 


11.70 


32 


16.39 


7.84 


48 


24.59 


11.79 




16.65 


7.99 




24.85 


11.95 


33 


16.91 


8.13 


49 


25.10 


12.09 




17.16 


8.23 




25.36 


12.18 


34 


17.42 
17.67 


8.38 
8.47 


50 


25.62 


12.23 


35 


17.92 
18.18 


8.62 
8.71 









OF THE URINE. 29 

Causes of Variation in the Amount of Urea. — In 
general, urea is increased whenever the supply of 
nitrogen to the body or the body metabolism itself 
is increased. Such causes may be stated in tabu- 
lar form, thus: — 

UREA. 
Increase. Diminution. 

Nitrogenous diet. Vegetable diet. 

Ingestion of compounds of am- Chronic diseases in general. 

monium. 

Excessive mental or physical Dropsical conditions. 2 

exercise. 

Nervous disturbances. Liver diseases. 3 
Excessive drinking. 

Active stage of acute disease. 1 Recovery from acute disease 

Gout. (nitrogen going to repair the 

wasted tissues). 

Diabetes mellitus. 4 Onset of death. 
Diabetes insipidus (especially). 4 

Substances allied to Urea. 

Kreatin is a normal constituent of muscle tissue, 
but not of the urine. It is intimately related to 

1 Intermittent fever an exception. Urea is increased in the 
interval between the paroxysms. Vide p. 11. 

2 In dropsical conditions the urea passes into the effusion, and 
as this is reabsorbed, the urea, increases. 

8 In disease of the liver, the urea bears a direct proportion to 
the working capacity of this organ. In acute yellow atrophy 
the urea is diminished, because it is eliminated prematurely as 
leucine and tyrosine. 

4 An exception to the rule for chronic diseases. Vide p. 13. 



30 CLINICAL EXAMINATION 

Kreatinin, which is a normal constituent of the 
urine. By the addition of a single molecule of 
water, kreatinin becomes kreatin, Kreatinin is 
found in the urine only after the ingestion of ani- 
mal foods has begun. 

Sarkine, Xanthine, and Uric Acid are interme- 
diate products of oxidation on their way to urea. 
Sarkine has no clinical importance. Xanthine, 
combined with uric acid, may form a constituent 
of urinary calculi. It is also present in the lungs 
and spleen. If xanthine and nitric acid be eyap- 
orated to dryness, and potassic hydrate added 
thereto, a pinkish color changing to purplish blue 
is deyeloped, — so-called murexide test. 

Uric Acid (U) is present, normally, in small 
amount, — J gram in twenty -four hours. It mar 
be increased to four grams ; but such an increase is 
due to abnormal conditions of the system, and is 
independent of dietary influences. 

Uric acid is a more complex substance than 
urea ; one molecule of uric acid splitting up, under 
certain circumstances, into two molecules of urea 
and a compound of oxalic acid. In the urine of 
the carniyora, e. g. birds and reptiles, uric acid 
replaces urea as the chief nitrogenous excretion. 
It is a weak dibasic acid, and occurs in human 
urine, not as a free acid, but combined with-the 
alkaline bases sodium and potassium, and to a less 
extent with calcium and ammonium. 



OF THE URINE. 31 

The metabolic changes in the albuminoid tissues 
result in the formation of uric acid (H 2 U). In 
the blood it meets the alkaline sodic phosphate, 
and the following reactions occur: 

NaaHP0 4 + H 2 U = NaH 2 P0 4 + HNaU; 
Na 2 HP0 4 + HNafj = NaH 2 P0 4 + Na 2 U. 

The products of the second reaction pass with ease 
through animal membranes, and therefore appear 
in the urine. 

By oxidation uric acid passes into urea. There 
are, however, intermediate steps, in which alloxan 
and parabamic, oxaluric, and oxalic acids are 
formed. 

If nitric acid be added to uric acid, alloxan and 
urea are formed. The reduction of alloxan gives 
alloxantin. Ammonium hydrate, when added to a 
mixture of alloxan and alloxantin, gives murex- 
ide. The murexide reaction forms the chief test 
for uric acid. A similar reaction, however, is ob- 
tained from xanthin with potassic hydrate. If 
heat be applied, the color if due to uric acid 
promptly disappears, whereas if due to xanthin 
it increases in intensity. 

In alkaline solution uric acid is a powerful re- 
ducer. If paper moistened w4th silver nitrate be 
dipped in an alkaline solution of uric acid, metal- 
lic silver is deposited on the paper. This reduc- 



82 CLINICAL EXAMINATION 

tion is even more marked with solutions of copper. 
(Compare Trommer's test for sugar.) 

Tests. — If a little hydrochloric acid be added to 
a test-tube half filled with urine, in the course of 
twenty-four hours crystals of uric acid will be 
found on the sides and bottom of the tube. A 
sufficient and quicker clinical test will be men- 
tioned under Tests for Albumen. 

Variation in the Amount of Uric Acid. — It is 
sufficiently evident, inasmuch as urea represents 
the final product of complete oxidation and uric 
acid only one of the intermediate stages, that any 
cause whereby oxidation is hindered will give rise 
to an increased elimination of uric acid. Such 
is found to be the case especially in pneumonia 
(li-2 grams in 24 hours) ; also in pulmonary tu- 
berculosis, chronic gout, acute rheumatism, and 
lung and heart diseases accompanied by dyspnoea 
and indigestion. Under conditions of health, 
when the amount of urine is diminished, the uric 
acid may be relatively increased. 

Uric acid forms two classes of salts, the neutral 
and the acid. The former are readily soluble 
in water, the latter considerably less soluble, 
whereas uric acid itself is almost insoluble, al- 
though, like the acid salt, more soluble in hot than 
in cold water. If for any reason there exists in 
the economy a diminished supply of bases or an 



OF THE URINE. 33 

over supply of uric acid, the latter will fall out 
of solution and appear as a sediment in the urine. 
Such a separation occurring in the course of the 
urinary passages gives rise to " gravel, " which in 
turn may act as the starting point of " stone or 
calculi." 

Hippuric Acid forms only a small constituent of 
human urine, but in the urine of the herbivora it 
occurs in large quantities, and appears to supply 
the place of uric acid. It is derived more or less 
directly from the constituents of the food contain- 
ing substances belonging to the aromatic series 
(benzoic acid or its radical). The benzoic acid 
meets glycocoll, a constituent of the body, and. hip- 
puric acid is formed. There is reason to believe 
that this change is in part accomplished through 
the activity of the renal epithelium. 

It is detected by the same test as that employed 
for uric acid, but hippuric acid is soluble in hot 
alcohol, whereas uric acid is not. Hippuric acid 
does not respond to the murexide test. 

Variation in the Amount of Hippuric Acid. — It 
is increased by a diet of vegetables or substances 
containing the benzoic acid radical, e. g. such 
fruits as greengages and whortleberries. Hippuric 
acid is also increased in diabetes, in which disease 
it more or less replaces uric acid. Finally, if ten 
grains of benzoic acid be taken at night, in the 



34 CLINICAL EXAMINATION 

morning crystals of hippuric acid will be found in 
the urine. 

Phenol (phenylic acid, carbolic acid) is never 
found as such in normal urine, but as a salt of 
phenol-sulphuric acid. It is to this substance, of 
which 15-20 mg. are eliminated in the twenty- 
four hours, that the pleasant odor of fresh urine is 
mainly due. 

Among the products of intestinal fermentation 
are. phenol, indol, and skatol, of which phenol is 
found in the intestine between the other two, i. e. 
indol being formed higher up, while skatol is 
formed lower down in the intestine. The condi- 
tions, therefore, that give rise to phenol and indol 
are identical, except that indol is formed earlier 
in point of time. A portion of the phenol may be 
obtained from the feces, while the rest finds its 
way into the urine. 

After absorption into the system, phenol as such 
disappears, for it meets sulphuric acid, and phenol- 
sulphuric acid, which is not poisonous, is formed. 
[The proper antidote for carbolic acid poisoning, 
then, is an alkaline sulphate with which the phenol 
may combine to form the phenol-sulphuric acid. ] 

When present in excess, phenol imparts to the 
urine a dark color, which may not appear until 
after the urine has left the body and stood a while* 
If the presence of phenol in the system is suspected. 



OF THE CRINE. 35 

it is an important step to test the urine for the 
sulphates. If phenol is present, the sulphates will 
of course be absent. 

The test for phenol : when boiled with a solu- 
tion of calcic hypochlorite, phenol imparts a green 
color to the solution. 

In peritonitis and septic diseases, the phenol of 
the urine is increased. Under the same condi- 
tions, indoxyl is also increased. In fact, they 
follow each other very closely. 

The Coloring Matters of the urine are nor- 
mally two : urobilin and indoxyl. 

Urobilin (hydrobilirubin, urohsematin, uro- 
phjeix) is derived more or less directly from the 
blood. The decomposition in the liver of the 
haemoglobin of the blood gives rise to bilirubin, 
which, as a constituent of the bile, passes into 
the intestine. Here it is reduced by the action of 
water and nascent hydrogen (hydrogen is a pro- 
duct of intestinal fermentation and represents 
50% of the total gases), and urobilin is formed. 
This is then absorbed and excreted by the kidneys. 
Thus, the direct descent of urobilin from the blood 
is established. It would appear, then, that the 
amount of urobilin in the urine might be taken 
as a measure of the decomposition of the blood, 
and such appears to be the case; for diseases in 
which there is an increased destruction of the blood 



36 CLINICAL EXAMINATION 

globules are characterized by an increase both in 
the bile pigment and the urobilin of the urine. 
Jaundiced urines contain, besides free bile pig- 
ment, an increased amount of urobilin. 

Urobilin in concentrated alkaline solution pos- 
sesses a dark brown color, and in dilute solutions 
a rose-red or pinkish hue. For practical purposes 
the color is graded to a system of units, of which 
15 corresponds to that normally found in the 
urine. In acute disease (typhoid and typhus fevers) 
the color may rise as high as 60. 

Urobilin is set free by sulphuric acid, and up- 
on this fact is based Heller's test for urophcein. 
About 2 c. c. of colorless sulphuric acid is poured 
into a collamore wine-glass, and into it, from a 
height of four or five inches, twice as much urine 
is allowed to fall. The urine mingles intimately 
with the acid, and if the amount of urophaein is 
normal a deep garnet-red color is at once devel- 
oped. If the urophaein is increased, the color 
developed is black and opaque; if diminished, it 
is paler, wine-red, and more or less transparent. 
It should be remembered that urine containing 
sugar, blood, or bile pigments gives an apparent 
increase of urophaein. It is also curious to note 
that the ingestion of potassic chlorate causes a 
diminution of the color reaction. 

Uroxanthin was the name given by Heller to 



OF THE URINE. 37 

the well known substance indican (of the Indigo 
group). It has now been found that, as a coloring 
matter of the urine it is not indican, but indoxyl 
(an oxidized product of indol), and that it exists in 
the urine as a sulphate. It is not, properly speak- 
ing, a urinary pigment, but under certain condi- 
tions it may be decomposed with the liberation of 
indigo, the latter imparting to the urine a blue or 
violet color. This decomposition may occur high 
up in the urinary passages, and so give rise to the 
dirty blue urine previously alluded to (page 17). 

In the course of pancreatic digestion, or as a 
result of intestinal fermentation, indol is formed. 
This is absorbed into the blood where by oxidation 
(one atom of 0) it is changed to indoxyl. It then 
pairs off with sulphuric acid to form indoxyl-sul- 
phuric acid, and subsequently indoxyl sulphate of 
potassium. The last, when heated out of contact 
with the air, splits into potassic sulphate and sul- 
phuric acid. When oxidized, it changes to the 
acid sulphate of potassium and indigo-blue ; under 
certain conditions, to indigo-red. Skatol is formed 
late in the digestive processes, and is found in the 
faeces. It is believed that skatol contributes to the 
formation of indigo-red, but how is not at pres- 
ent known. At all events, skatol is quite analo- 
gous to indol, and between the two an intimate 
chemical relation exists. 



38 CLINICAL EXAMINATION 

Heller's test is performed as follows: 4 c.c. of 
pure hydrochloric acid are poured into a collamore 
wine-glass, and to it are added about 20 drops 
of urine. The mixture is stirred, and, if the 
amount of indoxyl present be normal, a delicate 
amethystine color is developed. The test is ren- 
dered more delicate if 2 or 3 drops of nitric acid 
are added first. If iodide of potassium has been 
ingested, the addition of the HN0 3 is unnecessary, 
as iodine, which is itself a powerful oxidizer, is 
liberated. According as the amount of indoxyl 
present is more or less than normal, so wall the 
intensity of the color vary. 

Variation in. the Amount of Indoxyl. — A decrease 
of indoxyl is not pathological. It simply indi- 
cates a dilute urine. Indoxyl is increased in those 
conditions in which intestinal digestion is so in- 
terfered with as to cause an increased formation of 
indol. Normally the urine of twenty -four hours 
contains 5-20 milligrams of indoxyl. This may be 
increased, notably in peritonitis, to 100 mg. There 
is also a large increase in cholera. Furthermore, 
indoxyl is increased in simple fever, obstructive 
disease of the small intestine, chronic diseases, 
such as malignant disease of stomach or liver, 
rickets, pulmonary consumption, amyloid degener- 
ation of kidney (if associated with consumption), 
chronic interstitial nephritis, Addison's disease, 



OF THE URINE. 39 

phenol poisoning, septic diseases, and diseases in 
which nerve tissue is being destroyed. It is also 
increased by an exclusively meat diet, after coitus, 
and following the ingestion of indol. Grossich 
declares that in every case of fracture, or other 
bone lesion, the urine contains an excess of in- 
dican, and suggests that in doubtful cases it should 
be looked for. Finally, there may be a relative 
increase due to concentration of the urine, e. g. in 
hot weather. 

With increased indoxyl, there is always an as- 
sociated increase of phenol. 

Normal Inorganic Constituents. 

The inorganic salts exist in the urine, for the 
most part, in natural solution, the composition of 
the ash corresponding very closely to the results 
of direct analysis. The ash for 24 hours is from 
10 to 20 grams. The chief bases are sodium, 
potassium, calcium, and magnesium. There are 
traces of iron and silicon. These appear to be 
combined, for the most part, with hydrochloric, 
phosphoric, sulphuric, uric, and hippuric acids. 

Chlorides (CI). — Chlorine combined with sodi- 
um to form sodium chloride is the most abundant 
inorganic constituent of the urine. There are 
also small quantities of potassium and ammonium 
chloride present, but the amount is so insignificant 



40 CLINICAL EXAMINATION 

that they may all be considered together. In 
health, the chlorides of the urine correspond almost 
exactly with the amount taken in with the food. 
The quantity recovered from the urine in 24 hours 
is not far from 10 to 12 grams. 

Tests. — Heller's clinical test is based on the fact 
that a solution of nitrate of silver throws down, in 
acid solution, the chloride of silver. A collamore 
wine-glass is half filled with urine. A few drops 
of nitric acid are added (otherwise the addition of 
the silver nitrate is liable to precipitate the phos- 
phates as well as the chlorides) to render it acid ; 
then from a pipette or dropper is allowed to fall a 
single drop of the silver nitrate solution (1 part 
to 8). As a result, if the quantity of chlorides is 
not diminished, chloride of silver in the form of a 
white cheesy lump is at once formed in the urine. 
If the chlorides are slightly diminished, then the 
cheesy lump which forms slowly disintegrates, giv- 
ing the urine a more or less milky look. If they 
are diminished to -^ of \oJ or less, a simple 
cloudiness follows the addition of the AgNCL 
Finally, should no precipitate occur, the chlo- 
rides are probably absent. 

The quantitative test is a volumetric one, devised 
by Mohr. There are required : — 

1. Cold saturated solution of neutral chromate 
of potassium. 



OF THE URINE. 41 

2. A solution of silver nitrate, such that 1 c.c. 
= 10 mg. NaCl. [Dissolve 29.075 grams pure fused 
silver nitrate in distilled water, and dilute to a 
litre.] 

Process. — Ten c.c. of urine are put into a plati- 
num crucible, and two grams of potassium nitrate 
(free of chlorides) added. The mixture is slowly 
evaporated over the water-bath to dryness. The 
residue is heated, at first gently, then intensely, 
until the carbon is completely oxidized (residue 
white). The crucible is then placed in a beaker 
of water to dissolve the slag. When this is dis- 
solved, the crucible is removed, and washed off 
with a wash-bottle, care being taken that the 
wash water flows into the "slag solution." The 
solution is then made slightly acid by dilute ni- 
tric acid (free of chlorine) and again neutralized 
by a pinch of calcium carbonate. To this mix- 
ture, without regard to the sediment, two or three 
drops of the potassium chromate solution are 
added, and the silver solution allowed to run in 
from the burette until a distinct red color re- 
mains. [The silver combines preferably with chlo- 
rine. When, however, all the chlorine has been 
consumed, it unites with the chromic acid radical 
to form chromate of silver. This, being red, colors 
the fluid, and indicates the point at which all the 
chlorine present has united with the silver. ] The 



42 CLINICAL EXAMINATION 

amount of silver nitrate solution used is then read 
off from the burette, and the quantity of chloride 
calculated as follows. Suppose exactly 8 c.c. of 
the silver solution were used. Since 1 c.c. AgXO* 
solution = .010 gram chloride (or 10 mg. ), 8 c.c. 
= .080 gram, and since 10 c.c. of urine (the 
amount used in the test) contain .080 gram, 1500 
c.c. (or the amount passed in 24 hours) contain 
.080 X Ho"? or 12 grams. 

Variation in the Quantity of Chlorides. — There 
is no pathological increase of chlorides. They are 
diminished in all acute febrile conditions, espe- 
cially if there is an exudation of which they form 
a part. As soon as the exudation ceases and ab- 
sorption begins, they increase, or, if absent, re- 
appear in the urine. It may therefore become at 
times a matter of some clinical importance to test 
the urine for chlorides, e.g. in acute pneumonia. 
In this disease the chlorides may wholly disappear 
from the urine after the third or fourth day. 
Their reappearance would then indicate the criti- 
cal or turning point of the disease. 

In all other acute febrile diseases accompanied 
by serous exudation or watery diarrhoea, — pleu- 
risy, peritonitis, meningitis, acute rheumatism, 
pyaemia, and septicaemia, — or chronic diseases ac- 
companied by dropsy, the chlorides are diminished. 
As an aid in differentiating typhoid fever from 



OF THE URINE. 43 

meningitis, it may be said that the chlorides dis 
appear from the urine with greater rapidity in the 
latter disease. 

Phosphates. — The phosphoric acid of the urine 
is divided between the alkalies (Na and K) and 
alkaline earths (Ca and Mg) forming the so-called 
alkaline and earthy phosphates. The amount of 
phosphoric acid excreted in the 24 hours is from 
3 to 3* grams, of which two thirds are in combi- 
nation with the alkalies. 

The Earthy Phosphates (E. P. ), namely, calcium 
and magnesium, constitute only a small proportion 
of the total phosphates. Of this proportion about 
two thirds is magnesium, and one third is calcium 
phosphate. Both are present as the acid salt, — 
CaHP0 4 and MgHP0 4 ; and both are soluble in 
acids, but insoluble (the Mg salt, however, is 
slightly soluble) in water. 

In nearly neutral urines, boiling decomposes the 
phosphates, viz. : 

4 CaHP0 4 = Ca 3 (P0 4 ) 2 + CaH 4 (P0 4 ) 9 

(Heated.) (Soluble in alkaline solution) 

Lest the precipitate thus formed should be mis* 
taken for albumen, it is customary in the heat test 
for this substance to add a few drops of acetic acid 
to keep the phosphates in solution. 

Detection. — To a test tube half filled with clear 



4 -i CLINICAL EXAMINATION 

(filtered) urine, a few drops of amnionic hydrate 
are added. Upon warming the mixture, the earthy 
phosphates separate out and in 10 or 15 minutes 
settle to the bottom of the tube. If the deposit 
thus formed is from ^ to ^ an inch deep, the 
amount may be said to be within normal limits. 

In normal urine the earthy phosphates are pre- 
cipitated white, but if the urine contains an abnor- 
mal pigment, — blood, bile, or vegetable coloring 
matter, — they carry down the pigment with them, 
and so may be variously colored. Vide Color of 
Urine, p. 16. 

The Alkaline Phosphates (A. P.), viz. sodium 
and potassium, are present almost wholly as acid 
salts. They are soluble in water, and, unlike the 
earthy phosphates, are not precipitated by alkalies. 
The acidity of the urine is due in large measure to 
the acid sodium phosphate. 

Detection. — To the filtrate (in another test 
tube) of the earthy phosphates, about one third as 
much of the magnesian fluid (saturated solution 
MgS0 4 -j- NH 4 C1) is added. A white precipitate 
of the alkaline phosphates occurs, which settles 
to the bottom of the tube. If the precipitate is 
from J to | inch deep, the quantity is normal. 

Qualitative Test, — volumetric process. — The so- 
lutions required are : — 

1. Sodium acetate solution. 100 grin. NaA are 



OF THE URINE. 45 

dissolved in 900 c,c. of water, and 100 c.c. acetic 
acid added. 

2. Nitrate of uranium solution, so made that 
1 c.c. corresponds to 5 milligrams of phosphoric 
acid. 

3. Solution of potassic ferrocyanide. 

Process. — 50 c.c. of urine and 5 c.c. of the so- 
dium acetate are warmed together over the water 
bath. To this the uranium solution is added drop 
by drop as long as a precipitate is observed, or 
until a drop of the urine mixture, when brought 
into contact with a piece of filter paper wet with 
the ferrocyanide, develops a brown color. The 
number of c.c. used (uranium solution) multiplied 
by 0. 005 will give the quantity of phosphoric acid 
in 50 c.c. of urine. From this the amount con- 
tained in the twenty-four-hour urine is readily 
calculated. 

Variations in Quantity of Phosphoric Acid. — 
(The inferences are drawn from the acid alone. ) 

Bony and nervous tissues contain phosphorus, 
and their destruction by disease will be accompa- 
nied by an increase in the phosphates of the urine. 
Lung tissue also contains phosphorus, and in the 
early stages of phthisis the phosphates of the urine 
are increased. An increase is also noticeable in 
polyuria, and especially after the ingestion of phos- 
phatic food or salts of phosphorus. A diurnal 



46 CLINICAL EXAMINATION 

variation of the phosphates, corresponding closely 
to the normal daily variation alluded to in connec- 
tion with the quantity of the urine, is said to 
exist. 

A persistent excess of phosphates in the urine is 
termed phosphaturia. Inasmuch as this condition, 
in which the amount of phosphates may reach as 
high as 7 to 10 grams in the 24 hours, gives rise to 
symptoms not unlike those of saccharine diabetes, 
it was formerly called phosphatic diabetes. With 
phosphatiiria, glycosuria may or may not coexist. 
In case such a combination exists, an increase of 
sugar is accompanied by a decrease of the phos- 
phates, and vice versa. 

Sulphates (Sf). — These appear in the urine as 
the result of the oxidation of sulphur compounds 
(albumens contain S), chiefly in the form of the 
neutral sulphates of sodium and potassium. The 
normal daily excretion lies between 2 and 4 grams. 
Any sulphate taken into the body is completely 
eliminated in from 18 to 20 hours. 

Test — To J a test tube of urine, one third as 
much of the barium solution (saturated solution 
BaCl 2 + \ HC1) is addled. A white precipitate 
falls, which, if it fills one half the concavity of the 
test tube, may be considered normal in amount. 

Variation in the Quantity of Sulphates. — The in- 
gestion of sulphur, or any salt or fluid (mineral 



OF THE URINE. 47 

waters) containing it, will be followed by an in- 
crease of the sulphates in the urine. They are also 
slightly increased, following the urea very closely, 
whenever the metabolic processes are increased. 

The sulphates are diminished whenever there is 
a poor appetite, when phenol has been absorbed 
into the system, or when any substance is present 
that will unite to form a sulpho-acid. 

In the ordinary clinical analysis of the urine, it 
is not important to test for the presence of the sul- 
phates, except when poisoning by phenol is sus- 
pected. ( Vide Phenol, p. 34. ) 

Abnormal Constituents. 

The abnormal constituents of the urine consist 
chiefly of albuminous, saccharine, and coloring 
matters. In addition to these, various other sub- 
stances, representing either the products of im- 
paired metabolism or the elimination unchanged of 
many mineral substances, are frequently present 
in varying amount. 

Albumen in the Urine constitutes the symptom 
albuminuria. This is not per se diagnostic of or- 
ganic renal disease. Recent investigation shows 
that it is a remarkably frequent, and at times per- 
sistent, symptom in many persons apparently in 
good health. Although undesirable, it cannot in 
itself be always regarded as a grave symptom. 



48 CLINICAL EXAMINATION 

The forms of albumen usually found in the urine 
are egg and serum albumen. Closely allied to 
these, but differing in some of their reactions 
are : — 

1. The globulins, four in number ; vitellin, myo- 
sin, fibrinogen, paraglobulin. They are insoluble 
in water, soluble in dilute neutral saline solutions. 

2. Acid and alkali albumen. They are formed 
in the one case by the action of dilute acids, and 
in the other by alkalies on native albumen. Heat 
will not coagulate either of them, and each is sol- 
uble only in the solution designated by its name. 

3. Peptone. This form is soluble in water, but 
is not coagulated either by heat, acids, or alkalies. 
It is not normally found in urine, but when pres- 
ent, the symptom is termed peptonuria. Formed 
as a result of gastric and pancreatic digestion, 
peptone may find its way into the urine through 
various channels resulting from suppurations. It 
is also said to be present in the urine when pus cor- 
puscles are disintegrating anywhere in the body. 

Furthermore, pus and seminal fluid contain a 
small trace of albumen. Mucin, although not pre- 
cipitated from solutions by boiling, is coagulated 
by dilute acetic acid. 

After all, it is only important to be familiar 
with serum albumen ; further consideration of the 
other forms of albumen becomes unnecessarv. 



OF THE URINE. 49 

[As a constituent of the blood, albumen may ap- 
pear in the urine as a result of hemorrhage or 
transudation from some portion of the urinary pas- 
sages below the kidneys, — false albuminuria.] 

Detection. — The most satisfactory clinical tests 
for albumen in the urine are the heat and nitric 
acid tests. The urine should be rendered perfectly 
clear by filtration. If it does not filter readily, it 
is customary to separate the earthy phosphates 
by the addition of ammonia. These, in falling, 
carry down the bacteria and other annoying sub- 
stances, after which filtration is usually readily 
accomplished. Should the urine be already alka- 
line, it may be rendered filterable by the sepa- 
ration with the magnesian fluid of the alkaline 
phosphates. 

Heat Test. — Albumen in solution is coagulable 
at about 70° C. Therefore, if a test tube half full 
of urine be heated carefully to a temperature just 
below the boiling point, albumen, if present, will 
be precipitated, and the clear solution rendered 
turbid or cloudy, according to the amount of albu- 
men present. But heat is also liable, especially 
in urine whose reaction is close to the neutral 
line, to precipitate the earthy phosphates which 
may be mistaken for albumem Hence it is cus- 
tomary to add a few drops of acetic acid, either 
before or after the heating, to keep the phosphates 

4 



50 CLINICAL EXAMINATION 

in solution, and thus insure against such a source 
of error. If the acetic acid be added before heat- 
ing, it is not unlikely that a slight precipitation 
of mucin will occur. If, on the other hand, the 
acid is not added, and on heating no coagulum 
appears, one step in the process has been saved. It 
is always advisable to confine the heating to the 
upper half of the fluid, as any cloudiness in this 
half, however slight, can thereby be readily com- 
pared with the clear, unheated portion below. In 
this way, the heat test becomes a fairly delicate 
means of determining the presence of albumen. 

It should not be forgotten, however, that a few 
drops of nitric acid or an excess of acetic acid 
may convert the serum albumen into acid albumen, 
which is not coagulated by heat. Hence it may 
happen that (a) a precipitate of albumen may be 
dissolved by the addition of a few drops of nitric 
acid (although it reappears when an excess has 
been added), and (b) although much albumen is 
present it will fail to coagulate by heat if a few 
drops of nitric acid have been previously added. 
Although acid albumen is readily precipitated on 
neutralization with potassic hydrate, yet the least 
excess of alkali converts it into alkali albumen, 
and it redissolves. Hence it is dangerous to sub- 
stitute nitric for acetic acid in this test. 

Nitric Acid Test — This test operates equally 



OF THE URINE. 51 

well with serum, acid, or alkali albumen. It is 
also serviceable as an approximate quantitative 
test. 

A collamore wine-glass is filled about half full 
of urine. To this is carefully added nitric acid, 
allowing the latter to flow down the side of the 
wine-glass, which is gently inclined to facilitate 
the operation. As the acid is heavier than the 
urine, it settles en masse in the lower portion of the 
glass, while the urine overlies it. 

If albumen is present, it appears as a faint (or 
dense) white cloud or coagulum, forming a zone be- 
tween the urine and the acid. To insure detection, 
after the addition of the acid it is well to hold 
the glass against some dark background, as the 
sleeve of a black coat. By so doing, very slight 
traces of albumen will not be overlooked. 

If now the zone is thin, and, looking down upon 
it, quite transparent, the presence of a small 
amount of albumen (^ of \°J by weight, or less) 
may be assumed. Should the zone be thin (about 
the thickness of a crow-quill), opaque, but not 
flaky, it is indicative of about \ of 1%. Finally, 
if the zone is of the thickness of a goose-quill, 
opaque and flaky, the quantity is probably not 
far from | of \°j . The maximum amount of 
albumen ever present in the urine is 3 or 4 per 
cent by weight 



52 CLINICAL EXAMINATION 

The nitric acid test is valuable, clinically, for it 
not only indicates the approximate quantity of al- 
bumen present, but also betrays the presence of 
some other constituents as well. E. g. : — 

1. In urine that contains an excess of urates, 
it is likely that another zone, above the albumen, 
(or where it would be if present,) will be observed. 
This zone, as suggested, consists of the mixed acid 
urates and uric acid that have been rendered less 
soluble by the addition of the nitric acid. This 
forms a sufficient clinical test for uric acid. 

2. On the other hand, a zone in the nitric acid, 
below the albumen, consists of nitrate of urea, and 
is suggestive either of an excess of urea or a highly 
concentrated urine. 

3. Should any bile pigment be present in the 
urine, between the urine and the acid the charac- 
teristic play of colors will be observed. 

4. Having performed the test for albumen, in 
the same glass a drop of silver nitrate may be 
added, and any increase or diminution of the chlo- 
rides ascertained. 

On account of the possibilities of error, it is al- 
ways advisable, in testing for albumen, to perform 
both the heat and the nitric acid tests. By so do- 
ing, it is hardly possible to overlook the presence 
of albumen. 

Under certain conditions, viz. in testing jaun- 



OF THE URINE. 53 

diced urine, or where there is a large excess of 
urates present, it is preferable to employ the 
heat test. The same is also true when iodine 
or any resinous substance is present. If iodine 
is present, a brown-colored granular zone, which 
might easily mask a faint trace of albumen, is 
developed between the layers of acid and urine. 

There are many other tests for albumen, — picric 
acid, sodium tungstate, nitrate of mercury (Millon's 
reagent), sulphate of copper (biuret), etc. , — each 
serviceable in its own way; none of these, how- 
ever, are of any clinical importance. 

Finally, before testing for any of the normal 
constituents except the phosphates, it is well to 
remove any large excess of albumen. 

Albuminuria may be renal (true), or non-renal 
(false). 

True albuminuria depends mainly upon a dis- 
turbance either of blood pressure in the glomeruli, 
or of the nutrition of the glomerular walls. Any 
cause, therefore, that excites a disturbance of 
the diffusion membranes of the kidney, will be 
productive of albuminuria. Hence it happens 
that severe muscular or mental exertion, cold 
bathing on rising from bed, and even the inges- 
tion of food, give rise to a temporary or "func- 
tional " albuminuria, that cannot be regarded as 
in the least pathological. Albuminuria of this 



54 CLINICAL EXAMINATION 

nature may be intermittent (i. e. every morning), 
paroxysmal, or even persistent. 

Between the ages of fifteen and twenty there is 
frequently observed a temporary albuminuria asso- 
ciated with a physiological hypertrophy of the 
heart. This phenomenon is known as the albumi- 
nuria of adolescence , and is physiological. 

When urine is passed in small quantity, of high 
specific gravity, and contains crystals of calcic ox- 
alate, it is very liable to be slightly albuminous. 

False albuminuria arises in consequence of hem- 
orrhage into the urinary passages somewhere belotv 
the kidneys. It is essential, therefore, to bear in 
mind always the possibility of such a source of 
albumen. 

Pathologically, albuminuria arises under a va- 
riety of conditions. In many instances it seems 
to be an associated symptom of general constitu- 
tional (especially febrile) disease, i. e. scarlet fever, 
diphtheria, and other disturbances of an infectious 
nature. In other cases, it appears to be associated 
with a true poison that is circulating in the blood, 
e. g. cantharides, iodoform, etc. In such cases, it 
is not unlikely that the albuminuria is due to irri- 
tation of the kidney caused by its attempt to elim- 
inate the poison from the system. 

Albuminuria appears, also, when for any reason 
the outflow of blood from the kidney is hindered, 



OF THE URINE. 55 

e. g. in emphysema, phthisis, uncompensated val- 
vular disease of the heart, and those conditions 
accompanied by general passive congestion; also 
in ovarian tumors, uterine tumors (pregnancy), or 
new growths, so situated as to obstruct the venous 
outflow of the kidney. 

Finally, albuminuria is a most important symp- 
tom of organic disease of the kidneys themselves. 

In acute parenchymatous nephritis during the 
acute or inflammatory stage, the amount of albu- 
men in the urine varies from \ to 1|%. As the 
inflammation subsides and the amount of urine 
begins to increase, the albumen gradually dimin- 
ishes to a trace, and finally disappears. 

In chronic parenchymatous nephritis during the 
active stage, the amount of albumen is excessively 
large, — \-^°/o ordinarily \ to 2%. In the inactive 
stage it varies from \-\°fo. 

In chronic interstitial nephritis, the albumen 
rarely reaches |%. It is usually |%, more or 
less. 

In amyloid degeneration of the kidney it begins 
as a mere trace, and steadily increases, — \-\°Jo 
usually, but may rise as high as 3%. 

In active hyperemia of the kidneys, the amount 
varies with the blood pressure ; usually less than 
^%, oftener about ^q%, but it may temporarily 
rise as high as \of . 



56 CLINICAL EXAMINATION 

In passive congestion the amount varies with 
the degree of obstruction; i. e. anywhere up to \oj , 
but it is rarely more than a trace. 

Sugae. — The presence of sugar in the urine 
constitutes the symptom glycosuria. It is doubt- 
ful whether sugar is a normal constituent of the 
urine. In health, however, the quantity present 
never exceeds ^ of 1%, and in Trommer's test 
(vide page 58) it fails to make any impression 
upon the copper salt. Therefore this very small 
quantity may be disregarded. When the body 
contains an excess of sugar, it becomes a constit- 
uent of those fluids and tissues of the body nor- 
mally free from it ; at the same time, the amount 
of sugar in those tissues and fluids normally con- 
taining it is correspondingly increased. 

There are several chemical varieties of sugar, 
namely, milk, cane, grape, and fruit, but that 
which finds its way into the urine is grape sugar. 
Grape sugar is also known under the name of 
glucose, dextrose, starch sugar, diabetic sugar, 
etc. 

Pure grape sugar is as harmless an article of 
diet as any form of food, but it is not a satisfac- 
tory substitute for the common cane sugar. 

Glucose is made by the action of sulphuric acid 
on starch ; hence the name starch sugar. It turns 
polarized light to the right, and upon this fact is 



OF THE URINE. 57 

based a most satisfactory, though expensive, quan- 
titative test. 

Detection. — The specific gravity alone, when 
1030 or more, is quite suggestive of the presence 
of sugar ; and if at the same time the urine is very 
pale, and exceeds 1500 c.c. in the 21 hours, the 
probability that sugar is present becomes almost 
a certainty. The only presumptive source of error 
is a large excess of urea. 

Moore's or Heller's Test. — When heated with a 
fixed alkaline hydrate, grape sugar becomes a pow^- 
erful reducing agent. Melassic acid is formed, 
and a deep brown color is imparted to the solution. 
If a few drops of nitric acid be added to this, the 
dark color vanishes, and an odor of molasses is 
liberated. 

Process. — Pour into a test tube two volumes of 
urine and one of KOH, and heat to boiling. (If 
the earthy phosphates are present in excess, they 
may be removed by filtration. ) Presently, if sugar 
is present, the dark color appears, and deepens on 
standing. 

According to Bodecker, if a urine is treated with 
KOH and allowed to stand in the air, it gradually 
colors brown from above downward, because of the 
presence of a substance which he calls alkapton, 
Alkapton is a powerful reducing agent, and ab- 
sorbs oxvgen from the air. It will not reduce 



58 CLINICAL EXAMINATION 

bismuth salts, nor does it respond to the fermenta- 
tion test. Hence, in performing the copper test, 
it may be necessary to remove the alkapton with 
basic acetate of lead. 

Trommer's Test. — This is like the former, except 
that, before heating, a solution of cupric sulphate 
is added drop by drop, shaking after each addi- 
tion until a beautiful azure-blue color is developed. 
Upon heating, the copper sulphate parts with some 
of its oxygen, and orange-yellow cuprous oxide is 
formed. 

The precipitate must be obtained ivithout boiling. 
Both of the above tests will react without heat, but 
they then require ten or twelve hours. Ammo- 
nium salts, urea, albumen, and organic substances 
generally, tend to hold the cuprous oxide in solu- 
tion, and so interfere with the delicacy of the test. 
Then, again, other substances beside sugar act as 
reducing agents to the copper salt ; viz. uric acid, 
urates, hippuric acid, hypoxanthin, mucus, in- 
doxyl, urochloralic acid (after the ingestion of 
chloral), and turpenoglycuronic acid (when turpen- 
tine has been taken). 

Inosit, or muscle sugar, is widely distributed 
throughout the body. Although not a normal 
constituent, it may make its appearance in the 
urine, either replacing or accompanying the grape 
susrar. It has been found in the urine of acute 



OF THE URINE. 59 

nephritis, also in phthisis, syphilitic cachexia, and 
typhus fever. Inosit docs not reduce the copper- 
salt in solution with KOH, but in place thereof a 
green color is developed. Neither does inosit re- 
spond to the fermentation test (vide infra). 

Fehling's Test is simply a modification of that 
suggested by Trommer, and is subject to the same 
sources of error. It is, however, the one commonly 
employed in making quantitative estimations of 
sugar. Fehling's solution consists of a solution of 
pure crystallized sulphate of copper (34.639 grm. 
to 200 grm. dist. water), to which is added, a little 
at a time, chemically pure neutral sodic tartrate 
(173 grm.) dissolved in 500 grm. of a solution of 
caustic socla (sp. gr. 1.12). The clear mixture is 
then diluted to a litre. 10 c. c. of this solution 
will be reduced by 50 milligrams of diabetic su- 
gar. With a view to overcoming the extreme 
liability of Fehling's solution to decompose on 
keeping, it may be suggested that the solution of 
copper and that of the tartrate in the caustic soda 
be kept in separate bottles until required for use. 

Quantitative Estimation. — Pour into a flask 10 
c.e. of the freshly mixed Fehling's solution and 
40 c. c. of distilled water. Place the flask with its 
contents on the sand bath, and heat to boiling. If 
the specific gravity is over 1030, the urine should 
be diluted 1 : 10 ; if under 1030, the dilution need 



60 CLINICAL EXAMINATION 

not be so great, e. g. 1 : 5. The diluted urine is 
then placed in a burette, the level of the fluid 
brought to the zero mark, and the beak of the bu- 
rette inserted into the neck of the flask. Now, 
drop by drop, the urine is added to the boiling so- 
lution below, until the last trace of blue color dis- 
appears. (If, on boiling, the Fehling's solution 
changes color before the suspected urine is added, 
it will be necessary to obtain a fresh supply. ) 

The number of cubic centimeters of diluted 
urine used is then read off; e. g. 5 c. c. Inas- 
much as the urine was diluted, say 1 : 10, there 
must have been § c.c. of undiluted urine used in 
performing the test. 

Now, since 10 c.c. of Fehling's solution (the 
amount used) corresponds to . 050 grm. sugar ; the 
\ c.c. of urine necessary to the reduction must 
therefore have contained just this quantity, viz. 
.050 grm. sugar. Hence 1 c.c. of urine will 
contain .050 X 2 = .10 grm. sugar; or 100 c.c. 
10 grm. =10%. From these data the amount in 
24 hours is readily calculated. 

Fermentation Test. — By fermentation, sugar is 
broken up into alcohol and C0 2 ; therefore it is 
only necessary to cause fermentation in the urine, 
which can be done by the addition of a little yeast- 
cake. The C0 2 as it forms is passed through 
barvta water. 



OF THE URINE. 01 

A more useful application of the fermentation 
test is in the so-called "Differential Density 
Method," suggested by Dr. Roberts. It is founded 
on the fact that (a) during fermentation diabetic 
urine suffers a diminution of density due to the 
destruction of the sugar; and (b) according to 
Dr. Roberts's observations each degree of dimi- 
nution corresponds to one grain of sugar per fluid 
ounce. 

Process. — Two four-ounce bottles are filled with 
saccharine urine. A small piece of yeast-cake 
is added to one, and the bottle, loosely corked, 
is put in a warm place. The other bottle is 
tightly corked, and placed in some cool spot. 
After standing two days, the specific gravity of the 
urine in each of the bottles is taken; then each 
degree of difference will represent one grain of 
sugar per fluid ounce. The percentage may be 
approximately determined from the result thus ob- 
tained by multiplying the number of degrees lost 
in the fermentation by 0.23. 

Bottger's Bismuth Test is open to the objection 
of being too delicate. Sugar reduces nitrate of 
bismuth with the precipitation of metallic bis- 
muth (black). All organic albumens contain sul- 
phur, and are liable to cause the formation of black 
sulphide of bismuth, and so obscure the test. It is 
therefore imperative that, previous to performing 



62 CLINICAL EXAMINATION 

the test, all traces of albumen should be carefully 
removed. 

Brake's modification of the bismuth test is the 
most delicate of all. It is not, however, suffi- 
ciently practical to be given in this manual, and 
the reader is referred to more extensive works on 
the subject. 

Polarirnetry is one of the most reliable of tests, 
but the expense of the necessary instrument makes 
it unavailable for clinical practice. 

The presence of sugar can, in most cases, be 
satisfactorily determined by Moore's, Trommer's, 
Fehling's, or Roberts's (fermentation) test. 

Temporary glycosuria may be due to cerebral 
disturbance, carbonic acid poisoning, febrile dis- 
ease, especially pneumonia, or to the exhibition of 
certain chemical substances, e. g. turpentine and 
chloral. It may also occur in nursing women 
after weaning, or when the milk is not removed 
with sufficient rapidity. 

Pathologically, glycosuria characterizes the dis- 
ease diabetes mellitus. The amount of urine 
passed in 24 hours is greatly increased. It is pale 
in color, clear when passed, acid in reaction, and 
of high specific gravity. Together with a varying 
amount of sugar (3 or 4 to 10 or 12 per cent), the 
normal solid constituents, although absolutely in- 
creased, are, by the excess of water, relatively 



OF THE URINE. 63 

diminished. In this disease two or three pounds 
of sugar may be passed in 24 hours. 

Saccharine urine, on standing, becomes cloudy 
and more or less opaque from the growth of the 
sugar spore, Torula cerevisice ; but it does not be- 
come alkaline, and this is in part due to the pres- 
ence of acetic acid, and in part to the fact that a 
film forms over the surface of the urine, and pre- 
vents the entrance of the ordinary fermentation 
spore, Pencilium glaucum. 

In cases of glycosuria it is of importance to 
know whether the sugar in the urine varies with 
the amount ingested. For instance, during a pe- 
riod of fasting, the urine of a diabetic may contain 
a constant though very small amount of sugar, but 
upon resuming a starchy or carbohydrate diet this 
amount at once increases to 2 or 3^. Therefore, 
the increased glycosuria must be dependent upon 
the ingestion of food. Such cases are amenable 
to treatment, and the prognosis is not therefore 
wholly unfavorable. When, however, indepen- 
dently of diet, the glycosuria remains tolerably 
constant, the prognosis is unfavorable ; for in such 
cases the sugar eliminated in the urine must be at 
the expense of the permanent tissues. 

Leucine and Tyrosine are the decomposition 
products of the albuminous bodies or their de- 
rivatives. They appear to be present in the glan- 



64 CLINICAL EXAMINATION 

dular organs of the body, — liver, pancreas, and 
spleen, — especially when these organs are under- 
going pathological changes. They are associated 
as a crystalline sediment in the urine whenever 
the oxidative processes connected with tissue me- 
tabolism are for any reason hindered ; e. g. acute 
yellow atrophy of the liver, phosphorus poisoning 
(a few instances), typhus fever, and small-pox 
(occasionally). 

Abnormal Coloring Matters. 

These may be distinguished as (a) those which 
occur normally in other fluids of the body, as the 
blood and bile ; and (b) those which are the result 
of accidental excretion in the urine, viz. vegeta- 
ble coloring matters. The latter were sufficiently 
treated under the physical properties of the urine. 
(Vide Color, page 16.) It only remains to state 
that their presence is readily recognized from the 
fact, that, on the addition of an acid, the urine 
loses its color, which returns, however, when an 
excess of ammonia is added. 

Biliary Constituents. — When for any reason 
the bile cannot pass out of its channels into the 
intestine, it is reabsorbed by the blood, and elimi- 
nated by the kidneys, causing a discoloration of 
the urine, — an early symptom of jaundice. Clini- 
cally, only the coloring matters of the bile are 



OF THE URINE. 65 

important. The bile acids are never present in 
any considerable amount, and their significance 
when found is entirely out of proportion to the 
difficulties in the way of detecting them, since 
Pettenkofer's test is not available. 

The biliary pigments are several in number, and 
represent successive stages of oxidation through 
which the normal bilirubin passes. When present 
in excess, the urine is usually colored a deep brown 
or yellowish green, and when shaken with air a per- 
manent froth of yellowish green color is developed. 
A piece of filter-paper or linen, moistened with 
jaundiced urine, is permanently stained yellow. 

Bilirubin is always obtained from biliary cal- 
culi, in which it exists as a salt, insoluble in 
alcohol, chloroform, or ether. Cholesterine is 
separated by heating with ether, the lime is de- 
composed by the addition of hydrochloric acid, 
and bilirubin is freed. 

Jaundiced urine, when acidulated and shaken 
with chloroform, yields the biliary pigments to 
that reagent. 

Alkaline urine containing bile pigment turns 
green upon standing, owing to the formation of 
biliverdin from bilirubin by the absorption of an 
atom of oxygen. 

Grmelirfs Test consists simply in oxidizing the 
bilirubin with HN0 3 (the more impure, the better). 

5 



66 CLINICAL EXAMINATION 

The result is a play of colors in the following or- 
der: green, blue, violet, red, and yellow. It has 
already been noticed {vide page 52) how the test 
may be obtained during the nitric acid test for 
albumen, and generally the presence of a little 
albumen rather improves the test. Before apply- 
ing the nitric acid test, a very dark urine should 
be diluted with water. 

Another method is to add to a little urine, 
spread on a small porcelain dish, a drop of nitric 
acid. Prismatic rings of color are developed as 
above. 

There is no pathological increase of pigments. 
Their presence is indicative of jaundice, but 
they give no information as to the cause of the 
jaundice. 

Bile pigments adhere very readily to precipi- 
tates ; hence amorphous urates and the earthy 
phosphates precipitated from biliary urine are 
colored brown. 

Coloring Matters of the Blood. — An admix- 
ture of blood with the urine is easily recognized, 
unless the amount be very small, by the color. 
Haemoglobin is readily decomposed, by reducing 
agents and acids, to haematin and globulin (or 
globin). Haematin imparts a brown color to its 
solution. In an intermediate stage, methaemoglo- 
bin is formed, and this substance gives to its 



OF THE URINE. 67 

solution a darker shade of red than haemoglobin. 
According, then, as it is unaffected, or has under- 
gone decomposition, haemoglobin imparts to the 
urine a blood-red, brownish, or dark brown tint. 

Blood may enter the urine at any point, from 
the glomeruli to the external meatus. Naturally, 
that which enters the urine during its passage 
through the kidney, e. g. haemorrhages from the 
renal capillaries, is longer retained in the urine 
at the body temperature. This fact, combined with 
the absence of oxygen and the presence of carbonic 
acid, favors the decomposition of the blood to 
methaemoglobin and haematin, and the urine is 
therefore colored dark brown. The blood that en- 
ters the urine below the kidneys is less liable to 
undergo decomposition, and from this fact it fol- 
lows that the urine is more liable to be blood-red 
in color. As the blood undergoes decomposition, 
intermediate shades of color, according to the stage 
of decomposition, exist; and in order that the 
above distinction as to probable source may be 
made intelligently, it is necessary to observe the 
color of the urine at the time it is passed. 

Blood pigment in the urine may or may not be 
accompanied by the corpuscular elements. Rup- 
ture of the vessels, by which all the constituents of 
the blood escape into the urine, gives rise to the 
symptom hematuria. In such cases, the globules, 



68 CLINICAL EXAMINATION 

deprived more or less of their pigment, are de- 
tected in the sediment, while the colored urine 
betrays the presence (in solution) of the liberated 
pigment. 

In some diseases {vide infra) the blood is decom- 
posed while yet within the vessels, and upon its 
arrival in the kidney the pigment that has been 
liberated by this internal decomposition finds its 
way into the urine. Thus, the presence in the 
urine of the pigment, unaccompanied by corpuscu- 
lar elements, gives rise to the symptom of hcemo- 
globinuria. 

Hemoglobinuria is a symptom of scurvy, pur- 
pura, scarlatina, and profound malarial poisoning. 
It also occurs in septic and pyemic diseases, after 
the transfusion of blood from an animal of an- 
other species, after the inhalation of arseniuretted 
hydrogen, after severe burns, and after poisoning 
by many substances, viz. hydrochloric, sulphuric, 
and carbolic acids, and chlorate of potash. The 
urine is highly albuminous, colored brown, and in 
addition contains an abundant sediment of amor- 
phous matter. 

Like bile pigment, haemoglobin attaches itself 
to any precipitate ; e. g. if the albumen is coagu- 
lated, it is colored a distinct brown. At the same 
time, the urine loses the color due to the presence 
of blood, and assumes its otherwise normal tint. 



OF THE URINE. 69 

Undecomposed haemoglobin, together with me- 
thaemoglobin and haematin, may be detected with 
the aid of the spectroscope, or, if the quantity to 
be examined is very small, the microspectroscope. 
Oxyhemoglobin gives rise to two absorption 
bands, one in the yellow and the other in the 
green portion of the spectrum (i. e. between Fraun- 
hofer's lines D and E), while reduced haemoglo- 
bin gives only one band, situated between the 
two, which is fainter but broader than either of 
them. 

The disintegration of blood corpuscles within 
the body is accompanied by an increased activity 
of the liver. As a result of this, a larger quan- 
tity of bile pigment is secreted, which is elimi- 
nated in the urine with its usual pigmentary effect 
(cf. Urobilin). 

Tests for the Detection of Blood. — Teich- 
mari's test is very delicate. It is based on the 
fact that when haemoglobin is decomposed, haema- 
tin is formed. The latter readily unites with the 
halogens (CI, Br, I) to form haemin, the crystals 
of which are characteristic, and easily identified 
under the microscope. 

Process. — The earthy phosphates, to which the 
blood pigment readily attaches itself, are precip- 
itated and filtered out, dried, and a small quan- 
tity placed on a slide. To this are added a few 



70 CLINICAL EXAMINATION 

grains of common salt, and the two are then thor- 
oughly mixed. A hair is next laid across the 
mixture, and a cover-glass superimposed. A lit- 
tle glacial acetic acid is allowed to flow under 
the cover-glass, and the slide carefully warmed, 
until, under the cover, little bubbles appear. The 
slide is then set aside, and while it cools crystals 
of haemin form, which, as stated above, may be 
detected under the microscope. If, from too pro- 
longed heating, the crystallization is imperfect, 
a little more distilled water may be added, the 
slide warmed again, and then set aside for recrys- 
tallization. 

$odium Tang state Test — The urine is strongly 
acidulated with acetic acid, sodium tungstate 
added, and heat applied. A chocolate -brown pre- 
cipitate falls, with which Teichman's test is per- 
formed as above. 

The Heat Test. — Coagulation of the serum albu- 
men may be useful as a confirmatory test for blood. 
A drop of the suspected urine is placed on a glass 
slide and carefully heated. Coagulation of the 
albumen takes place, as in the heat test for that 
substance. 

The Iron Test is based on the fact that blood con- 
tains a little iron. The suspected precipitate is 
dried, and after ignition hydrochloric acid and po- 
tassic sulphocyanide are added. If iron is present 



OF THE URINE. 71 

(i. e. blood), a deep blood-red color is developed 
(ferric sulphocyanide). 

In cases of hematuria, the discovery of the cor- 
puscles with the aid of a microscope is the most 
reliable means of demonstrating the presence of 
blood in the urine. It should not be forgotten, 
however, that in very dilute or ammoniacal urine 
the blood disks may be dissolved, and so disappear 
quite rapidly. Hence failure to detect them does 
not invariably imply that they never were present 
in a given specimen. 

As will be shown in the chapter on sediments, 
the red blood globule, as found in urinary depos- 
its, varies in its optical appearances. It may be 
normal, or, owing to certain conditions (e. g. the 
presence of salts), distinctly abnormal. 

The microscopic test not only confirms the pres- 
ence of blood, and indicates its condition, i. e. 
whether normal or abnormal, but it also enables 
the skilled observer to determine from what animal 
the blood in question was derived. This follows 
from the fact that in different animals the diame- 
ter of the red corpuscle varies. In all the mamma- 
lia, except the camel and llama, the red corpuscle 
is circular or disk-shaped, and without a nucleus. 
In the cases just mentioned as exceptions, it is also 
non-nucleated, but oval in outline. On the other 
hand, in birds, reptiles, and fishes, it is both oval 
and nucleated. 



72 CLINICAL EXAMINATION 

The following table shows the average diameter 
of the blood disks of a few mammalia. 

Human, . . . . . -g^Vo inch. 

Goat .... -g-Y 1 ^ inch. Horse .... t ^ W q inch. 

Sheep .... T o^ " Pig ^30 " 

Dog ^0 " Cat ^ « 

Rabbit. . . . 3^0 " Squirrel . . . ^oo " 

For the purpose of measuring accurately the di- 
ameter of the disks, a microscopic slide, on which 
are ruled parallel lines yoV o" °^ an ^ nc ^ a P ar t? is 
used. The blood to be measured is placed on this 
slide and examined under a microscope, the ocular 
of which contains a scale so ruled that ten of its 
parallel lines correspond to the space between any 
two lines of the slide. Thus, a measurement of 

To o"o~o °^ an ^ nc k * s rea dily made, and the diame- 
ter of the globule in question easily determined. 

The best menstruum for preserving and mount- 
ing blood globules for measurement is acetate of 
potassium. 

Accidental Constituents. 

r Fat. — This may occur, in general, in one of 
four ways: — 1. The result of fatty degeneration 
of the cells lining the renal tubules. (A most 
important source.) 2. By the immediate con- 
nection of the lymphatics with the urinary pas- 
sages, giving rise to the so-called chyluria (vide 
next page). 3. By the direct separation of fat, as 



OF THE URINE. 73 

a result of renal activity. This occurs, but rarely, 
among pregnant women, and those taking a large 
amount of cod-liver oil. 4. By the accidental or 
intentional addition of extraneous fat, as may hap- 
pen after the passage of greased catheters and 
sounds ; from the use of old hair-oil bottles for 
transporting urine, etc. Hysterical patients may 
add oily substances to their urine for the purpose 
of deception. 

Fat is usually detected by its microscopic ap- 
pearances: globular outline and strongly refract- 
ing border; but even then it may at times (e. g. 
chylous urine) be a matter of some difficulty. 
Bubbles of air, too, often simulate fat globules 
extremely well. 

In the later stages of acute disease of the kidney 
fat may be present for a short time only. It is, 
however, a prominent symptom throughout the en- 
tire course of chfonic renal disease ; e. g. chronic 
parenchymatous nephritis. 

Fat may be present in the urine in a state of 
very minute subdivision, as in cliyhiria. Such 
a urine is spoken of as " chylous. " It is milky 
white in color, and the milkiness persists even on 
standing. Out of contact with the air, the fat 
does not separate out ; but on exposure decomposi- 
tion takes place, with the separation of the fat, 
which then rises to the surface. 



74 CLINICAL EXAMLNATION 

The addition of milk to normal urine produces 
an appearance resembling chyluria ; but under the 
microscope the fat globules of milk can be dis- 
tinguished, whereas those of chylous urine cannot. 
If chylous urine is shaken with ether, the ether 
takes up the fat. This is not so with milky urine, 
since the fat globule of milk is coated with an albu- 
minoid substance that must first be dissolved by 
the addition of an alkaline hydrate. 

Fat forms about 1% by weight of chylous urine. 
Besides the fat, considerable mucus, leucocytes, and 
blood globules are present. As elsewhere suggest- 
ed, the presence of chyle in the urine is probably 
due to a communication between the lymphatics 
and some point of the urinary passages. The com- 
munication is said to be effected by the action of a 
parasite, Filaria sanguinis hominis, which has been 
found in the blood of those afflicted with the dis- 
ease. The affection is quite common in the tropics, 
where it appears to be endemic. 

At times chyluria appears to be intermittent, 
i. e. occurring only in the morning, while daring the 
remainder of the day the urine is passed clear. 

Oholesterine may, though very rarely, be associ- 
ated with fat. Its presence in the urine is of little 
known significance, and of still less importance. 

Acids of the Fatty Series — formic, acetic, pro- 
pionic, butyric, etc. — are found in urine, but only 



OF TEE URINE. 75 

ill very small amounts. Acetic acid is present in 
the stage of acid fermentation, and in saccharine 
urine after fermentation has begun. In the latter 
instance, it is this acid that, in connection with 
the surface film {vide page 63), helps to prevent 
the urine from becoming alkaline. Butyric acid 
may be found in diabetic urine after the addition 
of chalk. The decomposition of leucine may give 
rise to the presence of valerianic acid. 

Of the Organic Acids which are not Fatty, lactic 
acid is present in urine in two forms. In diabetes, 
the ordinary lactic (milk) acid is present; but un- 
der certain circumstances sarqolactic acid may ap- 
pear. The only means of distinguishing the two 
forms lies in the fact that sarcolactic acid forms 
salts with zinc and calcium. 

Lactic acid is present, whenever the oxidative 
processes of the body are hindered, and therefore 
usually in connection with leucine and tyrosine ; 
viz. acute yellow atrophy of the liver, poisoning 
by phosphorus and arseniuretted hydrogen, typhus 
fever, and severe cases of small-pox. 

Benzoic acid is found in the urine of herbivora 
in abundance, as a result of the decomposition of 
hippuric acid. 

Ammonia Compounds. — Ammonia is normally 
present only in very small amount (1%). By diet 
and the decomposition of nitrogenous tissues some 



76 CLINICAL EXAMINATION 

variation in this amount may be induced. Carbo- 
nate of ammonium appears in urine as the result 
of the decomposition of urea. Sulphide of ammo- 
nium may appear whenever putrid suppuration is 
going on. 

Pus contains sulphur compounds, which, upon 
decomposing, it liberates. In any disease not con- 
nected with the urinary apparatus, the presence in 
the urine of sulphuretted hydrogen may be regarded 
as a favorable sign. 

Alkalies are present normally, and also as a 
result of medication. By the processes of body 
metabolism, citrates, tartrates, etc. are converted 
into and eliminated in the urine as carbonates. 

Iodide of Potassium may be detected when pre- 
sent by the nitric acid test for albumen. Between 
the two layers (urine and acid) a delicate brown- 
colored zone is formed (vide page 52). 

Extraneous substances, such as articles of food 
and drink, also various medicines, may get into 
urine, either accidentally or voluntarily (hysterical 
patients). As possible sources of urine contamina- 
tion, they should constantly be borne in mind. 

Various metallic salts, principally those of lead, 
arsenic, and mercury, are eliminated in the urine. 
In cases of suspected poisoning, their detection 
forms a very important set of urino-chemical 
analyses. 



OF THE URINE. 77 

Lead. — Unless means be taken to secure its 
removal, the lead that is absorbed accumulates in 
the system as a fixed constituent of the tissues. 
The natural channel of elimination is by way of the 
kidneys and urinary passages. In order that it 
should become a constituent of the urine, the lead 
must first be converted into a compound that is 
soluble in the blood. This is best effected by the 
administration of iodide of potassium. As this 
salt mingled with the blood circulates among the 
tissues containing lead, the latter is converted into 
plumbic iodide, a salt that is somewhat soluble in 
water at the temperature of the body, and is then 
carried by the blood to the kidneys, and eliminated 
as a constituent of the urine. Even under these 
circumstances, only a few milligrams of lead are 
eliminated in the twenty-four hours. It follows 
that, in order to detect its presence, a very large 
quantity of urine should be examined, and in the 
process of analysis every precaution taken to pre- 
vent the accidental addition of even the slightest 
quantity of extraneous lead. 

The Analysis. — A litre of urine is evaporated 
over the water bath to dryness. When nearly dry, 
the residue is moistened with nitric acid. When 
effervescence has ceased, the bright yellow resi- 
due is transferred while hot to a platinum cruci- 
ble, thoroughly heated, and ignited. The crucible 



78 CLINICAL EXAMINATION 

with its white residue is then placed in a dish of 
hot dilute hydrochloric acid to dissolve the slag. 
The solution is filtered while hot, and the filtrate 
treated with an excess of ammonia water and am- 
monium sulphide. This precipitates the phosphates 
and sulphides of iron and lead. After standing over 
night the precipitate is washed several times, by 
decantation, with boiling water, and an excess of 
hydrochloric acid added to dissolve the phosphates 
and sulphides of iron. After standing again over 
night, the sulphide of lead settles, and is then col- 
lected on Swedish filter-paper. The black sulphide 
of lead is washed with boiling water on the filter, 
after which boiling dilute (chemically pure) nitric 
acid is added, drop by drop. The sulphide dis- 
solves and is collected in a watch-glass. This is 
then evaporated to dryness over the water bath ; 
the result of which is a white residue of basic 
nitrate of lead. 

A preliminary test is first made by placing a 
crystal of the white residue in a watch-glass, and, 
after moistening with a drop of water, a crystal 
of potassic iodide is moved about in it. A yellow 
streak indicates the presence of some metal, prob- 
ably lead. The confirmatory test is performed as 
follows. The white residue (basic nitrate of lead) 
is dissolved in a drop or two of acetic acid, and 
washed with hot water through a filter-paper into 



OF THE URINE. 79 

a test tube. To this a drop of sulphuric acid is 
added, and by the next day sulphate of lead has 
formed. 

Arsenic. — The amount of arsenic eliminated in 
a litre of urine is very small ; hence, in the analy- 
sis for that metal, a considerable quantity of urine 
is necessary. 

Process. — One or two litres of urine are evapo- 
rated to dryness, moistened with nitric acid, and 
ignited (as in analysis for lead). The white resi- 
due from ignition is treated with dilute sulphuric 
acid, and heated strongly over a sand bath to expel 
any excess of nitric acid. The nitrates are con- 
verted by the process to sulphates, and these are 
extracted by water. The solution is then filtered, 
and the filtrate received into a Marsh's apparatus 
which has been previously tested and found to be 
free from arsenic. 

Mercury. — The urine is first concentrated to 
half its volume, and then acidified with dilute hy- 
drochloric acid. In this is suspended a platinum 
wire, to which is attached a bit of iron. After an 
hour or two, metallic mercury is deposited on the 
wire. The wire is then removed, rinsed with water, 
and suspended in an atmosphere of chlorine gas, 
by which the metallic mercury is converted into 
corrosive sublimate. The wire is then pressed 
between the fold of a paper which has been pre- 



80 CLINICAL EXAMINATION 

viously moistened with iodide of potassium. If 
mercury is present, a scarlet streak of mercuric 
iodide (Hgl 2 ) is left on the paper wherever it came 
in contact with the wire. 



OF THE URINE. 81 



CHAPTER III. 



THE SEDIMENT. 



A turbidity of the urine arises from the fact 
that it may, and often does, contain substances 
that are more or less insoluble in it. So long 
as these substances remain diffused through the 
fluid, turbidity persists. After a time, however, 
varying with the consistency of the urine and the 
weight of the insoluble matters, the latter gradu- 
ally settle to the bottom and form a sediment. In 
urinary examinations, the quantity of the sediment 
is usually reported as little {slighf), considerable , 
or much. 

The constituents of the sediment are eliminated 
from the body in the urine, either as such (i. e. al- 
ready separated), and have therefore only to settle, 
or, as the result of certain changes presently to be 
described, they may appear only after the urine has 
been passed. The changes referred to pertain more 
especially to the reaction of the urine, which after 
elimination undergoes modifications and change. 

When freshly passed, the acidity of normal urine 
is such that the solid inorganic constituents are 

6 



82 CLINICAL EXAMINATION 

kept in perfect solution. It has already been shown 
elsewhere, that certain of the urinary constituents, 
by the existence of a reaction other than of normal 
degree or kind, are rendered insoluble, and appear 
as deposits. Hence it follows that any considera- 
ble deviation of reaction from the normal will be 
followed by a precipitation of those constituents 
which are insoluble in urine of that reaction. Such 
changes of reaction may occur while the urine 
is yet within its natural channels (uric acid dia- 
thesis and cystitis), or only after it has been 
voided (fermentation). 

Fermentation of the Urine. 

When freshly passed, normal urine is perfectly 
clear ; but after standing a short time there ap- 
pears, floating somewhere between the top and 
bottom of the fluid, a faint nebula or cloud, com- 
posed of the mucus and exfoliated epithelium 
which, as the urine flows outward, are carried 
along with it. After longer standing, this nebula 
increases in volume and density, and finally set- 
tles to the bottom. The acidity of the urine, as 
well as the intensity of its color, has at the same 
time increased. In fact, the urine has undergone 
the so-called " acid fermentation." 

Two views are entertained with regard to the 
cause of the increased acidity. One theory is 



OF THE URINE. 83 

based on the tendency that exists between the 
acid sodium phosphate and normal urates to mu- 
tual decomposition, viz. : — 

1. Na 2 U + NaH a P0 4 == Na 2 KP0 4 -f NaHU. 

2. NaHU + NaH 2 P0 4 = Na 2 HP0 4 + H 2 U. 

Thus the acid sodic phosphate takes away a part 
of the base of the normal urate, and leaves the acid 
urate, which is less soluble than the normal salt. 
It is to the separation of this salt that the increase 
of the mucous cloud mentioned above is in part 
due. This reaction occurs especially at a low tem- 
perature ; but if the temperature be high, and at 
the same time there exists in the urine an excess of 
the acid sodic phosphate, the decomposition goes 
a step further. The acid urate salt is entirely 
deprived of its base, and the almost insoluble uric 
acid separates out as beautiful distinct crystals, 
which are reddish or reddish brown in color, and 
fall to the bottom as a granular powder. At times 
the uric acid is mixed with the amorphous unde- 
composed urates, forming the so-called brick-dust 
or lateritious sediment. 

The second theory is based on the fact that the 
coloring matters, through the agency of the mucus 
of the bladder acting as a ferment, are converted 
into acetic and lactic acids. These then react 
upon the normal urates in the same manner as the 



84 CLINICAL EXAMINATION 

acid phosphate of sodium, and with the same results. 
Sufficient proof that the fermentation assumed in 
this theory takes place is wanting, and therefore 
the first theory seems on the whole the more prob- 
able. 

When the changes described take place within 
the urinary passages, the urine, when passed, is 
turbid, and the sediment is spoken of as " gravel 
or sand." Such a condition is pathological, and 
paves the way to serious urinary disturbances. 

Mixed with the sediment that has fallen, as a 
result of the changes described above, are often 
found crystals of calcic oxalate. A part of the 
uric acid is in the organism changed to oxaluric 
acid, which on exposure to air becomes oxidized to 
oxalic acid, and appears in the sediment as calcic 
oxalate. 

When the decomposition between the urates and 
phosphates has ceased, there follows, after an in- 
terval which is much shorter in hot weather 
than in cold, a new process, — a true fermenta- 
tion. The color of the urine becomes paler, the 
reaction gradually less acid, neutral, and then 
alkaline. As a result of these changes, the uric 
acid and urates disappear and give place to a new 
series of salts, — phosphates of the alkaline earths. 
The odor becomes distinctly ammoniacal and then 
putrid, while the turbidity, now due to the presence 



OF THE URINE. 85 

of the alkaline phosphates and ever increasing mass 
of bacteria, constantly increases. 

To what the alkaline change is due, is a matter 
upon which authorities differ (vide Reaction, p. 18). 
According to some, it is believed that decomposing 
mucus liberates a ferment in the presence of which 
urea is decomposed. Others are inclined to re- 
gard the change as a species of bacterial fermenta- 
tion, while the remainder are inclined to the view 
that it proceeds from the action of a definite sub- 
stance or ferment, which can be isolated from alka- 
line urine (Musculus ferment, vide page 19). 

However effected, the fact remains that it is a 
true fermentative process, in which urea is decom- 
posed to carbonate of ammonium, and it is to the 
formation of this substance that the alkaline reac- 
tion is due. 

The ammonia can combine with uric acid to 
form urate of ammonium, which, unlike the other 
normal urates, is quite insoluble. This salt ap- 
pears in the sediment when ammonia is being set 
free, i. e. just at the beginning of the alkaline 
change, and before it joins with the magnesic 
phosphate to form the triple or ammonio-magnesic 
phosphate. 

Thus the changes in the sediment corresponding 
to the alkaline fermentation consist on the one 
hand in a disappearance of the salts formed in the 



86 CLINICAL EXAMINATION 

course of the acid fermentation, and on the other 
in the appearance of urate of ammonium (in the 
early stage), amorphous phosphate of lime, and 
triple phosphate, together with large quantities and 
numerous varieties of bacteria. 

As in the acid fermentation, so also in the alka- 
line, the change may take place within the body, 
i. e. pelvis of the kidney or bladder, and thereupon 
give rise to pathological conditions associated in 
the first instance with gravel or calculus, and in 
the second with irritation and inflammation, espe- 
cially of the bladder. 

Classification of the Sediment. 

Urinary deposits have been classified by different 
writers according to their physical characteristics, 
their nature and origin, and the reaction of the urine 
in which they are found. The simplest of these 
classifications is the second, in which the sediment 
is regarded either as organized or not organized. 

The organic deposit embraces all those organic 
forms which are insoluble in the urine, whether it 
is acid or alkaline. They are never normally pres- 
ent in urine, and when present are merely sus- 
pended in it, sinking more or less slowly to the 
bottom, and forming a part of the sediment. 

The non-organic deposit includes those sub- 
stances which, for the most part, exist in the urine 



OF THE URINE 87 

iii a soluble state. When for any reason, e. g. ex- 
cessive quantity or a change in the reaction of the 
urine, they are rendered insoluble, these substances 
are precipitated in a crystalline or amorphous con- 
dition. 

Following the classification suggested above, these 
substances may be tabulated as follows : — 



Non-organized. 


Organized. 


Uric acid. 


Mucus. 


i Na. 

Urates ^ 


Epithelial cells. 


l Ca an I Mg. 




Amorphous urates (mixed). 


Leucocytes and pus. 


Hippuric acid. 


Blood corpuscles. 


Calcic oxalate. 


Fibrin. 


Amorphous phosphates (mixed). 


Renal casts. 


Calcic phosphate. 


Spermatozoa. 


Triple phosphate. 


Fat. 


Calcic carbonate. 


Fungi. 


Cystine. 


Morbid growths. 


Xanthine. 


Entozoa. 


Cholesterine. 


Extraneous matter. 


Leucine. 




Tyrosine. 




Bilirubin (Haematoidin). 





Uric Acid and Urates. 

Uric acid, as has been said, exists in normal 
urine in combination with the alkaline bases, but 
under certain conditions it is itself precipitated as 
a reddish-colored deposit of small bulk, sinking to 
the bottom, or at times floating on the surface, and 
also adhering to the sides of the glass. 



88 CLINICAL EXAMINATION 

Uric acid is found only in acid urine (cf. Acid 
Fermentation, page 83). Causes contributing to its 
separation are those which induce a concentration 
of the urine, an increase of its acidity, or a patho- 
logical increase of uric acid. Uric acid and its 
salts when precipitated carry down the coloring 
matters present in the urine, and are therefore 
colored, usually a light yellow varying to dark 
brown, or under certain conditions amethystine. 
Pure uric acid is, however, white and amorphous. 
Owing to their free solubility, normal urates, except 
the ammonium salt, which is insoluble, are almost 
never present in sediment. The acid and its acid 
salts, however, are much less soluble, and therefore 
appear as very common constituents of urinary 
deposits. 

Recognition. — The typical or primary shape of 
uric acid crystals may be said to be a rhombic 
plate, to which the various forms met with may be 
referred. The angles and sides may be about 
equal, giving rise to quadrangular tables or cubes ; 
more frequently two opposite angles are rounded 
off, by which ovoid or whetstone crystals are ob- 
tained ; again, two opposite angles may be cut off 
smoothly, and so give rise to the hexagonal forms. 
Elongation produces a rod, and when many of these 
are joined about a common centre, fan-shaped to 
complete star forms are produced. Many other 



OF THE URINE. 



89 



atypical forms occur, whose recognition practice 
makes easy. 




Fig. 2. Various forms of Uric Acid Crystals. 

In general, crystals of uric acid are almost al- 
ways colored, insoluble in acids and hot or cold 
water, but soluble in alkaline hydrates. Finally, 
they respond to the murexide test (vide page 31). 
The hexagonal modification may be mistaken for 
cystine, but cystine is colorless, and soluble in hy- 
drochloric acid. The elongated rhombic prisms 
sometimes met with may be mistaken for crystals 
of triple phosphate, but the latter are colorless, 



90 CLINICAL EXAMINATION 

found only in ammoniacal urine, and are soluble 
in dilute acid. 

Urate of ammonium, as mentioned above, is an 
exception to the free solubility of the normal urates. 
It is very insoluble, and appears in urine after the 
liberation of ammonia has begun, i. e. at the begin- 
ning of the alkaline fermentation. It is the only 
urate found in alkaline urine, and crystallizes in 
the form of brown-colored spheres, either single 




Fig. 3. Spherules and Spiculated Spherules of Ammonium 
Urate and Amorphous Granular Urates- In the upper portion 
of the circle are Prismatic Crystals of Acid Sodium Urate. 

or double, and with smooth or spiculated surfaces. 
The characteristic appearance of the spheres when 
studded over with spines has given rise to the 



OF THE URINE. 91 

names hedgehog and thorn-apple crystals. If the 
spines are variously bent and distorted, a great 
variety of forms is produced. The elimination 
through the urinary passages of such crystals as 
these is frequently a cause of great irritation and 
pain. They may lead to the formation of calculi, 
and are commonly found in children whose urine 
is charged with renal calculi. 

The acid ammonium urate occurs only in alka- 
line urine, together with the earthy and triple 
phosphates. 

The acid urates are dissolved by heat and the 
alkalies ; also by dilute acids (e. g. dilute HC1) 
with subsequent crystallization of uric acid. They 
also respond to the murexide test. 

Occasionally the urates of sodium and potassium 
are crystalline, and appear in the sediment in forms 
resembling sheaves of wheat or delicate rosettes. 

The other urates (mixed) usually occur as a 
loose, amorphous, pulverulent reddish deposit 
(brick-dust sediment), separating usually after the 
urine has been passed. The color, of course, de- 
pends on the presence and intensity of the color- 
ing matters in the urine from which the urates are 
deposited. Microscopically, the deposit is indis- 
tinguishable from other fine granular matter, and 
therefore requires chemical tests to determine its 
nature. When attached to delicate shreds of mu- 



92 CLINICAL EXAMINATION 

cus, the amorphous urates may simulate fine granu- 
lar casts. With a little familiarity, however, their 
true nature is readily determined. 

The amorphous urates are soluble in hot, but 
insoluble (or less soluble) in cold water ; hence it 
happens that they often separate after the urine 
has cooled considerably below the body tempera- 
ture (as in cold rooms during the winter). The 
separation is of course more likely to occur when- 
ever there is a relative or absolute increase of the 
uric acid (concentrated and fever urines). 

Hippuric Acid. 

In conjunction with uric acid, and under condi- 
tions elsewhere stated (vide page 33), hippuric acid 
appears in the form either of prismatic acicular 
needles, or more commonly of semi-transparent 
quadrilateral prisms, with two or four bevelled sur- 
faces at their ends. They are distinguished from 
uric acid by the fact that they are colorless, do 
not respond to the murexide test, and are soluble 
in boiling alcohol. (Uric acid is not dissolved by 
boiling alcohol.) 

Calcic Oxalate. 

Among the oxidation products of albuminoid sub- 
stances (vide Acid Fermentation, page 84) is calcic 
oxalate. In sediments, calcic oxalate crystals usu- 



OF THE URINE. 93 

ally occur in two typical forms, i. e. quadrilateral 
octahedron and dumb-bell. The former is the 
more common form met with, and may be said 




Fig. 4. Various forms of Calcic Oxalate Crystals. 

to consist of two low four-sided pyramids joined 
at their bases ; hence their appearance varies ac- 
cording to the position in which they are viewed, 
e. g. envelope and diamond. Occasionally the two 
pyramids are joined by an interposed quadrilat- 
eral prism. In disintegrating, this part disappears 
first. 

The dumb-bell form is highly characteristic, and 
requires no further description. It may be men- 
tioned, however, that when seen end on, these 



94 CLINICAL EXAMINATION 

dumb-bell forms suggest oval-shaped crystals and 
biconcave disks, not unlike blood globules. 

Normally oxalic acid tends to undergo complete 
oxidation to carbon dioxide and water. It is also 
somewhat soluble in acid sodium phosphate; hence 
the small amount usually present is held in solu- 
tion. The amount of oxalic acid in the urine is 
increased by any interference with the normal ox- 
idative processes, or by the ingestion of oxalic 
acid in any form, e. g. rhubarb, garden sorrel, to- 
matoes and other vegetables, and carbonized drinks. 
Oxaluria, when persistent, gives rise to nervous 
symptoms somewhat analogous to those of ne- 
phritis, and it is therefore at times called "false 
Bright's disease." 

Finally, when separating in the renal tubules, 
the calcic oxalate crvstals give rise to considerable 
irritation ; the crystals become agglutinated in the 
consequent increased mucus secretion and so form 
the nuclei of renal calculi. 

Optical and Chemical Characters. — The only 
crystals with which calcic oxalate may be confused 
are the triple phosphate. The latter, however, oc- 
cur only in alkaline urine, and are readily dissolved 
by acetic acid, whereas calcic oxalate occurs only in 
acid urine and is unaffected by acetic acid. 

Crystals of uric acid and calcic oxalate are best 
preserved by washing (by decantation) with acetic 
acid. 



OF THE URINE. 95 

Earthy Phosphates. 

These consist of the phosphate of lime (amor- 
phous, Ca 3 (P0 4 ) 2 , crystalline, CaHP0 4 ), and the am- 
monio-magnesian or triple phosphate (MgNH 4 P0 4 . 
6 H 2 0). They occur as a bulky white opaque de- 
posit only in feebly acid or alkaline urine, and most 
abundantly in the urine of alkaline fermentation. 
The ingestion of vegetables which are largely alka- 
line is productive, within an hour or two, of a 
neutral or faintly alkaline urine, in which, if voided 
soon after a meal, is discovered a precipitate com- 
posed of earthy phosphates in an amorphous con- 
dition. In this state they do not tend to form 
calculi. 

The application of heat will at times, even in a 
slightly acid urine, by driving off the carbonic acid 
in which they are somewhat soluble, cause a pre- 
cipitate of phosphates which may be mistaken for 
albumen. The addition of acetic acid, however, 
will cause a solution and disappearance of the 
phosphates. 

The crystalline form of the phosphate of lime 
resembles very closely that of the acid urate of so- 
dium (i. e. rosette form). It occurs in weakly acid 
urine, either alone, or, as in alkaline urine, more 
commonly associated with the triple phosphate. 

Triple phosphate requires for its crystallization 



96 CLINICAL EXAMINATION 

the presence of ammonium compounds ; hence it is 
rarely found until the urine has, by the decompo- 
sition of the urea, become ammoniacal. The triple 
phosphate crystal is easily recognized as a trian- 
gular prism with bevelled ends. Owing to their 
characteristic shape, these crystals are also called 
" coffin-lid." Modifications occur in which one or 




Fig. 5. Coffin-lid Crystals of Triple Phosphates ; Feathery 
Star-shaped Crystals of the same At a is a group of Crystalline 
Phosphate of Lime 

more corners are wanting, or the body of the crys- 
tals is variously shortened. Such forms may be 
confused with calcic oxalate crystals, but may be 
distinguished as already stated (vide page 94). 
Occasionally, as when precipitated rapidly, beau- 



OF THE URINE. 



97 



tiful star-shaped feathery crystals of triple phos- 
phate are found. 

As a result of the alkaline changes that occur 
under certain conditions within the bladder, the 
earthy phosphates are deposited upon calculi of 
uric acid, calcic oxalate or ammonium urate. 

All the phosphates are soluble in acetic acid, 
whereas those salts resembling them are not. In 
case of doubt, this makes a ready test. 




Fig. 6. Spheres and Dumb-bells of Calcic Carbonate from the 
Urine of the Horse. (Roberts.) 



Calcic Carbonate. 

Crystals of this salt do not appear as an inde- 
pendent sediment, but associated with the earthy 
phosphates. Abundant in the urine of herbivora, 

7 



98 CLINICAL EXAMINATION 

it is present only exceptionally in man. Occurring 
usually as a fine-grained powder, it may assume a 
crystalline form not unlike urate of ammonium. 
It is, however, colorless, and upon the addition of 
mineral acids an effervescence occurs. 




Fig. 7. Cystine : Hexagonal Tablets and Prisms from an 
evaporated Ammoniacal Solution. (Roberts.) 

Cystine. 

Cystine is a crystalline body of considerable 
rarity. It is found only under certain abnormal 
conditions of the body, which are as yet but im- 
perfectly understood. The fact that it contains 



OF THE URINE. 99 

about 26% of sulphur suggests the possibility that 
it may be a vicarious secretion of taurin. 

Many instances are recorded in which cystinuria 
appears to be hereditary. 

Cystine crystallizes in regular hexagonal tablets 
of varying size, appearing either singly or in super- 
imposed series. The latter may be made up of crys- 
tals whose size diminishes in an ascending series, 
or of crystals which overlap each other like shin- 
gles on a roof. At times the opposite angles of 
the crystal are joined by lines passing through a 
common centre. Roberts mentions the occurrence 
of square prisms of cystine which refract light 
strongly, and in connection with the hexagonal 
form appear either singly or in stellate aggrega- 
tions. 

Like many other crystalline sediments, cystine 
is strongly disposed to separate inside the urinary 
passages and there give rise to calculi ; in this 
form cystine is more often found. 

Cystine can only be confounded optically with 
a pure, colorless, and exceedingly rare form of 
uric acid. By reflected light, however, the uric 
acid has a yellowish tinge, whereas cystine has an 
iridescent mother of pearl lustre. 

Chemical Characters. — Cystine is soluble in hy- 
drochloric, but insoluble in acetic acid ; hence the 
addition of the latter will precipitate cystine. It is 



100 CLINICAL EXAMINATION 

also soluble in ammonia, and the hydrates and 
carbonates of the fixed alkalies. By evaporation 
of the ammonia solution, beautiful hexagonal crys- 
tals of cystine may be obtained. If uric acid resem- 
bling cystine is dissolved in ammonia, then upon 
evaporation characteristic crystals of ammonium 
urate are formed. 

Xanthine. 

Xanthine is a very rare constituent of the sedi- 
ment. Like cystine, it occurs oftener as a con- 
stituent of calculi than as an independent crystal. 
It is so rare, that further consideration may be 
omitted. 

Cholesterine. 

Cholesterine, a crystalline derivative of fat, is an 
infrequent constituent of urinary sediments. It 
occurs in the form of long quadrangular plates 
of various sizes (Fig. 8), and is said to be present 
in fatty degeneration of the liver, and in cheesy 
cystic degeneration of the kidney 

Leucine and Tyrosine. 

In sediments these substances usually appear 
together, and since they accompany only grave de- 
structive diseases of the liver — acute yellow atro- 
phy and phosphorus poisoning — the urine is usu- 
ally highly charged with bile pigment. 



OF THE URINE. 



101 



When their presence is suspected, simple con- 
centration alone is sufficient to produce a sediment 
of leucine and tyrosine crystals. 




Fig. 8. Crystals of Cholesterine and Fatty Aggregations. 
(Roberts.) 

Under the microscope, leucine appears as more 
or less yellow-colored, refracting spheres of vari- 
ous sizes, which here and there show a disposition 
to aggregate, and, where the edges of two spheres 
come in contact, to fuse. They bear a strong re- 
semblance to oil drops, but are distinguished from 
them by their less strongly refracting border and 
insolubility in ether. Furthermore, when observed 



102 



CLINICAL EXAMINATION 



under suitable illumination, crystals of leucine 
exhibit in their interior a crystalline structure. 

Crystals of ammonium urate may resemble leu- 
cine spheres, but upon the application of heat the 



o^ 




Fig. 9. Leucine Spheres and Tyrosine Needles. 

former disappear. More frequently the urate of 
ammonium crystal is recognized by the spicules 
on its surface. 

Tyrosine crystallizes in delicate silky needles, 
arranged in tufts or sheaf-like aggregations, which 



OF THE URINE. 103 

occasionally cross each other at their middle con- 
stricted portions. 

Bilirubin (ELematoidin). 

Crystals of haematoidin are found in old blood 
extravasations and blood clots. Whenever any 
communication exists between such extravasations 
or clots and the urine, the haematoidin crystals may 
appear in the sediment. Under the microscope 
they appear as transparent ruby-red rhombic flakes, 
or as delicate needles varying in color from yellow 
to yellowish brown. 

Chemical Characters. — Haematoidin contains no 
iron ; is soluble in chloroform, but insoluble in 
water, alcohol, ether, and acetic acid. 

Organized Sediment. 

Mucus. 

Normal urine always contains a small amount 
of mucus and epithelium. The former is a normal 
secretion of the mucous membrane lining the uri- 
nary passages, and is therefore washed out by the 
flow of the urine ; the latter, as a result of the 
normal wear and tear to which the tissues are 
subjected, becomes loosened, and is also carried 
away by the urine. It is therefore a mistake to 
speak of urine as containing no sediment. Irrita- 



104 CLINICAL EXAMINATION 

tion or inflammation increases both these con- 
stituents, and by identifying the kind of epithelium 
which is present in excess, the seat of the inflamma- 
tory process may be determined. Simple irritation, 
however, such as may occur from a concentrated 
urine, increases at times only the mucus, which, 
since it is so transparent and similar to urine in 
its index of refraction, is recognized often only by 
other than its optical properties. 

By the action of acetic acid, mucin, which is a 
constituent of mucus, is separated as delicate fibril- 
lated bands, which at times are tortuous in outline 
and at other times appear as delicate threads. 

These mucus coagula often appear in urine to 
which no acid has been added, and in such in- 
stances are due to the action of acids developed in 
the course of the acid fermentation. 

Under the microscope these coagula appear as 
threads with pointed extremities and varying irreg- 
ularly in their diameter, whereas hyaline casts, with 
which they may be confounded, have a uniform diam- 
eter, increasing or diminishing symmetrically, and 
are usually rounded at the ends (Fig. 10). 

At times leucocytes, epithelium, and crystalline 
salts attach themselves to or become embedded in 
mucus, whereby it becomes more distinctly visible. 

When, as a result of irritation, the amount of 
mucus is largely increased, the urine becomes more 



OF THE URINE. 105 

or less viscid, and is designated " ropy." In addi- 
tion, cells from the seat of irritation are embedded 
in the mucus cloud, as stated above. 




Fig. 10. Mucus Coagula and Hyaline Casts. 

Leucocytes and Pus. 

Mucus is rarely present in any considerable 
quantity without being accompanied by more or 
less pus, as the causes which produce both differ 
simply in degree. Pus, however, contains albu- 
men, whereas mucus does not. Therefore, in a 
general way, it may be stated that the absence of 
albumen from a urine containing mucus is pre- 
sumptive evidence that pus is absent as well. 



106 CLINICAL EXAMINATION 

The presence of pus is determined microscop- 
ically by detection of the pus corpuscle in the sed- 
iment, Anatomically and in appearance the pus 
corpuscle and leucocyte (white corpuscle of the 
blood) are identical. It is customary, however, to 
use these terms with a quantitative significance. 
When only a few scattered corpuscles are present 
they are termed leucocytes, when present in large 
numbers they are called pus corpuscles. The pus 
corpuscle, as it appears in urine, is a small, granu- 
lar, more or less spherical cell, rather larger than a 
blood disk (i. e. about 10 \x in diameter), and con- 
taining one or more nuclei. It thus resembles very 

closely the round epithe- 
t «s| lial cells ; but the latter 




© <S) 



contain only one nucleus, 

fo\ which is quite distinct, 

whereas the pus corpus- 

Fig. 11. Mucus and Pus Cor- de contain several, 

puscles, before and after the ad- 

dition of acetic acid. (Tyson.) which, however, are not 

always easily discernible 
until acetic acid has been added. If a few drops of 
the acid be allowed to flow under the cover-glass 
upon pus corpuscles, they swell, are freed of their 
granular contents, and the nucleus or nuclei come 
out with great distinctness. Pus from the seat of 
an old inflammation often exhibits, when acted up- 
on by acetic acid, a characteristic nucleus of horse- 



OF THE URINE. 107 

shoe shape. It probably represents the fusion of 
several nuclei. 

Caustic alkalies have a characteristic and pro- 
nounced action upon pus. They destroy its mor- 
phological identity, and convert it into a viscid 
gelatinous mass. To this fact is due the " ropy " 
character which alkaline urine, containing pus in 
considerable quantity, assumes. Upon the same 
fact is based the test of Donne, whereby the pres- 
ence of pus in urine which is still acid is estab- 
lished. After settling, the deposit in which pus 
is suspected is separated by decantation from the 
supernatant urine. If pus is present, this deposit 
is converted, by the addition of amnionic or sodic 
hydrate, into a cohesive gelatinous lump. 

The commonest sources of pus in the urine are 
inflammations of the renal pelvis, bladder, prostate, 
and urethra. In each instance, except cystitis, the 
urine is usually acid, aud the presence of pus is 
determined by Donne's test. As a result of the 
ammoniacal changes incident to cystitis, the urine 
may become " ropy " while yet within the blad- 
der, and so plug the urethra as to cause all the 
distressing symptoms of obstructive anuria. ( Vide 
page 134.) 

The presence of pus often clears up a doubt con- 
cerning the identity of bladder or vaginal cells, for 
pus is associated most frequently with the former, 



108 CLINICAL EXAMINATION 

although purulent and leucorrhoeal discharges from 
the vagina may lead to the presence of vaginal cells 
and pus in the urine. 

The association of mucus and pus together with 
cells from the seat of irritation renders it impor- 
tant to determine next the characters by which 
the genito-urinary epithelium may be identified. 

The Epithelium. 

To describe the epithelium which may appear 
in the urine, it is necessary to have a unit of ref- 
erence, and in addition, for the purpose of men- 
suration, an element which is both familiar and 
tolerably constant in size. The bladder cell has 
been adopted as the former, and the pus corpuscle 
as the latter. 

The epithelium of the hladder is composed of 
the largest cells found in the urinary passages. 
They are flat or plate-like, irregularly polygonal 
in outline, three or four times the diameter of a 
pus corpuscle, and contain a single nucleus. 

When present in excess, many of the bladder 
cells are in single layers and adherent by their 
edges. This serves to differentiate them from vagi- 
nal cells, which they resemble. Besides being on 
the average somewhat larger, vaginal cells, when 
aggregated in masses, appear upon careful focusing 
to be made up of several distinct and overlapping 



OF THE URINE. 



109 



layers. Moreover, it is somewhat difficult to dis- 
tinguish the individual vaginal cells. 

From the bladder, both toward the external 
meatus and the kidney, the individual cells of the 
successive tissues progressively diminish in size. 




Fig. 12. Varieties of Epithelium. 

a. Two Leucocytes and a Blood Globule. 

b. Bladder Cells. 

c. Cells from Neck of Bladder and Prostate. 

d. Large and small Renal Cells ; the one at the right contains 
fat drops. 

e. Cordate Cells from the Renal Pelvis. 



The cells of the ureters are seldom met with in 
the sediment, and are of no great importance. 
Inflammatory processes, whether extending up- 
wards from the bladder, or downwards from the 
renal pelvis, apparently skip the ureters. Occa- 
sionally, however, as the result of the passage of a 



110 CLINICAL EXAMINATION 

calculus, the ureter cells are torn away and appear 
in the sediment. They are nucleated spindle-shaped 
cells. 

Cells from the pelvis of the kidney , according as 
they come from its superficial or deeper epithelial 
layers, are of two forms, — cordate and round. In 
acute inflammation of the pelvis the superficial 
layers are first detached, and are present in the 
sediment in excess. The individual cell has a 
cordate or battle-door outline, the head of which 
is about as large as a pus corpuscle, and contains 
the nucleus. Although somewhat unusual, they 
may appear in groups, the cells overlapping each 
other like shingles on a roof. This condition is 
more common when the inflammatory process has 
extended down from the kidney. 

After a few days of active inflammation, the 
cells of the deeper layers are detached. In size, 
shape, and appearance, they are like a renal cell, 
from which they cannot be distinguished. If from 
the pelvis, however, there is usually present in ad- 
dition some blood and an excess of pus corpus- 
cles, which are recognized by their multinuclear 
structure. 

The cells from the kidney are, as just stated, 
like those from the pelvis, but they vary more in 
size. If from the smaller renal tubules they are 
slightly smaller, and if from the larger tubules 



OF THE URINE. Ill 

they are somewhat larger, than a pus corpuscle. 
In addition, if the cells are of renal origin there 
are always present casts to which similar cells 
are attached, or in which they are embedded. At 
times the renal cells contain fat drops. 

In advanced stages of chronic parenchymatous 
nephritis, many of the renal cells undergo complete 
fatty degeneration, and appear in the sediment as 
more or less spherical aggregations of small fat 
drops. To these the name of compound granule 
cells has been given. {Vide Pig. 14, page 117.) 

The cells from the neck of the bladder and the 
prostatic urethra (male) resemble those of the blad- 
der proper. They are, however, smaller, denser, 
and generally rounder than the bladder cell. Sim- 
ilar cells occur in the female urethra, and are 
found in female urine under normal conditions. 

Below the prostate^ the cells are still smaller, 
both round and cordate, resembling those of the 
renal pelvis. If it is necessary to determine 
whether they are from the urethra (gonorrhoea, 
etc.), it is to be remarked that, when the urethra 
is inflamed independently of the bladder, the urine 
is cloudy at the beginning of micturition, and 
shortly becomes clear. In addition, there are 
present an excess of pus and more or less blood, 
while the cells are embedded in shreds of mucus, 
viz. gonorrhoeal threads. 



112 



CLINICAL EXAMINATION 



Blood Disks. 

The causes and general characters of the urine 
which suggest the presence of blood have already 
been discussed, and it now remains only to indi- 
cate the appearances by which these suggestions 
are confirmed ; viz. by recognizing the optical 
characters, as viewed under the microscope, of 




Fig. 13. Blood Disks. Those in the left half of the circle are 
normal, — those in the upper quadrant being crenated. Those in 
the right half are abnormal. 

the disks themselves. These differ according to 
the place at which they enter the urine, and the 
length of time that they remain in it. 

The disks that enter the urine below the kid- 
neys, and have therefore remained in the urine 



OF THE URINE. 113 

only a relatively short time, present a tolerably 
normal appearance. They are circular, biconcave 
disks of about one half the diameter of a pus 
corpuscle, and of a slightly yellow color. Their 
biconcave structure is proved by the alternation 
of light and shadow at the centre and periphery 
as the objective-glass of the microscope is ap- 
proximated to them. When seen on edge, the 
disks resemble a dumb-bell, and their biconcave 
structure becomes more evident. If the urine is 
a concentrated one, the disks shrink, and together 
with their diminution in size exhibit a crenated 
or irregular outline. They are still to be regarded 
as normal globules. 

When poured into the urine before it leaves the 
kidney, the disks undergo changes by which they 
lose their color and biconcave structure, diminish 
one half in size and become spherical, looking very 
much like a small, round ring. The disk in which 
these changes have occurred is to be regarded as 
abnormal. The same alterations occur in dilute 
ammoniacal urine, but with the increase of alkalin- 
ity the globules slowly disintegrate and are finally 
dissolved. 

Fibrin. 

Associated with blood, fibrin coagula may occa- 
sionally be found. These coagula are usually 



114 CLINICAL EXAMINATION 

colored by the action of blood pigment, and exhibit 
a vacuolar appearance, i. e looking as though some- 
thing had been shaken out of their interior. 

Renal Casts. 

The identification of renal casts is a most im- 
portant step in the diagnosis of renal disease. 
They are, as their name implies, casts or moulds 
of the uriniferous tubules, produced by the pres- 
ence in the latter of some coagulable matter. This 
material, as it sets, entangles in its substance what- 
ever debris is present in the tubules at the time, 
and, subsequently contracting a little, is washed 
out of the tubules into the renal pelvis, and thence 
to the bladder and urine receptacle. 

In general, true albuminuria is presumptive evi- 
dence of the presence of casts. There have been 
only a few isolated cases in which casts have been 
detected unaccompanied by albuminuria. 

Several theories as to the origin of casts exist. 
It goes without saying that in cases of renal hem- 
orrhage the blood may clot in the tubules and give 
rise to a fibrin cast. Three other theories of some 
importance, however, are to be entertained. 

1. The Transudation into the Tubules of some 
Coagulable Material, probably Albuminous, from 
the Blood. — If the renal vein of a normal kidney 
be tied, there results an oedema of the organ. If 



OF THE URINE. 115 

it then be put into boiling water and sections ex- 
amined, a homogeneous glistening material, which 
is chemically a fixed albuminate, will be observed 
in the lymph spaces and interstitial tissue. 

2. An Abnormal Product of Epithelial Secretion 
or Activity. — Similar suppositions are entertained 
with regard to the processes observed in many 
cases of thyroid goitre. 

3. A Product or Residt of Cell Degeneration. — 
In fresh sections of the kidney filled with casts, 
the material of which the latter are composed 
exhibits shadowy outlines suggestive of cellular 
origin. Hence it is possible to regard this co- 
agulated material as composed of disintegrating 
or wholly disintegrated cells, i. e. a kind of hy- 
aline degeneration. 

Whatever its origin may be, this homogeneous 
albuminoid material differs at times in its optical 
characters. It may be highly refractile, granular, 
and colored, or it may be perfectly clear, colorless, 
and of a refrangibility differing but slightly from 
that of the urine itself. 

It is perfectly obvious that, in the process of 
setting, any loose material, e. g. epithelium, blood 
disks, granular debris, etc., present in the tubules, 
is liable to become adherent to or embedded in the 
setting mass, and thus alter the appearance of the 
cast. Upon the changes so effected a classification 



116 



CLINICAL EXAMINATION 



of casts is based, although it is to be remembered 
that all casts, except perhaps the fibrin casts men- 
tioned above, are at base hyaline. 



Casts. , 



1. Hyaline, 

2. Epithelial. 

3. Blood. 

4. Fatty 



C pure. 

■} fibrinous. 

( waxy. 



5. Granular, 



/colorless 1 ne ' 
j ( coarse. 

( brown \ &ne - 

( coarse. 

„ _, „. ( uric acid and urates. 

6. Crystalline, < t . . x 

( calcic oxalate. 

7. Pus. 



In general, casts are recognized when viewed 
under the microscope by their more or less uni- 
formly cylindrical appearance and rounded ends. 
Their length is usually greater, and often several 
times greater, than their width. If their diameter 
diminishes, it is usually at one point (cf. Mucous 
Casts, page 105). 

At times casts have a divergent branch, i. e. 
Y-shaped, indicating their origin at some point 
where the second convoluted portion of the tubules 
enters the collecting or straight tubules. It is 
inconceivable how casts formed behind the nar- 
rowed descending loop of Henle, i. e. in the first 
convoluted portions, can be eliminated as formed 
in the urine. 



OF THE URINE. 



117 




Fig. 14. Varieties of Renal Casts. 

a. Epithelial, — a containing at its lower end a group of abnor- 

mal Blood Globules. 

b. Fine Granular. 

c. Fatty. 

d. Compound Granule Cells. 

e. Waxy. 

f, f. Pure Hyaline. 



118 CLINICAL EXAMINATION 

Hyaline Casts. — In the broad sense, hyaline 
means a clear homogeneous cast. This would in- 
clude the waxy and fibrinous casts, presently to be 
described ; hence it is better to use the prefix pure, 
as it restricts the term to those casts which are 
clear, homogeneous, and of slight refrangibility. 
They are often seen with difficulty, and may be 
overlooked unless the illumination of the field be 
modified by shading with the hand or by manipula- 
tion of the mirror itself. 

A waxy cast is in no way different from a pure 
hyaline, save that its diameter may be somewhat 
greater and its refrangibility much increased. It 
looks more solid, and not unlike molten wax. In 
fact, it bears somewhat the same relation to a 
hyaline cast that a fat drop does to an abnormal 
blood disk. 

A fibrinous cast is like the waxy, save that it 
is colored by blood pigment, usually, a yellow or 
yellowish brown. This form is usually accom- 
panied by isolated blood globules in the sediment. 
Its composition is not definitely known. It does 
not necessarily follow, however, that they are 
composed of fibrin. The name is probably a mis- 
nomer. 

The other casts are simply hyaline, with which 
different formed elements have become united; 
viz. epithelial, when holding renal cells ; blood, when 



OF THE URINE. 119 

blood disks are present ; fatty, when containing fat 
drops ; and granular, when containing granular 
debris. 

According to the color or absence of color, granu- 
lar casts may be brown or colorless ; according to 
the size of the granules, fine, medium, or coarse ; 
and according to the quantity, highly, moderately, 
or slightly granular. Brown granular casts are 
made up of disintegrated urates, blood globules, 
and epithelium, colored by blood pigment. The 
source and nature of the materials composing the 
coarse granular casts is as yet doubtful. They are 
commonly associated with waxy casts. 

Mixed casts are, as the name implies, those in 
which the different formed elements are associated 
in one cast. 

Crystalline casts are those in which the crystal- 
line matter, separating in the tubules, has been 
caught in the coagulating material. Such crystals 
are the urates, uric acid, and calcic oxalate. 

Pus casts may occur in the course of acute 
inflammatory conditions. In pyelitis and pyelo- 
nephritis the pus corpuscles are frequently agglom- 
erated in masses which are suggestive of casts and 
may come from the straight tubules. They are 
usually of considerable size, — much larger than 
the renal casts. 

Casts of the seminal tubules may appear, and 



120 CLINICAL EXAMINATION 

are recognized by the associated presence of sper- 
matozoa. 

Hints on the Examination for Casts. — Owing to 
their extreme lightness, casts settle slowly. The 
urine should be collected in a urine-glass (i. e. a 
more or less conical glass, having a rounded bottom 
and holding about a pint), covered with a glass plate 
and allowed to stand some twelve hours. To ob- 
tain a specimen, a pipette, made of glass tubing 
more than sufficiently long to reach the bottom, 
and drawn nearly to a point at one end, is used. 
With the fore-finger pressed firmly over the smooth 
proximal end, the pointed end is passed down to 
the sediment, which is seen in a mass at the bottom 
or on the sides of the glass near the bottom. Hav- 
ing selected a spot for trial, the fore-finger is raised 
an instant ; a little of the sediment rises up into the 
pipette, and the finger is clapped down again. The 
pipette is then carefully and slowly withdrawn, and 
while the finger is still pressed on the end, the 
point is wiped with a soft linen cloth. The sedi- 
ment in the point of the pipette is then placed on 
a glass slide by raising the fore-finger, and ex- 
amined under the microscope, using a tolerably 
high power (Zeiss Oc. 3, Obj. D). 

In case there is considerable sediment it is al- 
ways well to take specimens from different lay- 
ers, — top, middle, and bottom, — and never to feel 



OF THE URINE. 121 

satisfied with the examination of one specimen, 
unless a positive result is obtained. When there is 
a very slight sediment, it often attaches itself as a 
delicate film to the sides of the glass near the 
bottom. Specimens from this should be examined, 
first loosening, by scratching it, with the point of 
the pipette, and then collecting in the usual way. 
Success will often attend this procedure. 

Fat. 

The appearances and significance of fat in the 
urine have already been sufficiently treated {vide 
page 73). 

Spermatozoa. 

There are no characters imparted to the urine 
by spermatozoa which are perfectly characteristic 
of their presence. When present in abundance, 
they may form a delicate flocculent cloud in the 
urine, which under the microscope is resolved into 
a mass of spermatozoa embedded in a fine granular 
menstruum. The microscopic appearances of sper- 
matozoa, with their flattened pyriform body and 
long filamentous tail, are sufficiently well known, 
and require no further description. 

They occur in the urine of males suffering from 
spermatorrhoea, and after coitus, nocturnal emis- 
sions, etc. ; in the urine of females, after coitus or 



122 CLINICAL EXAMINATION 

attempted coitus. The recognition of spermatozoa 
in the latter instance may be a matter of considera- 
ble medico-legal importance, i. e. cases of suspected 
rape. With the exception of such cases, the exam- 
ination of the sediment for spermatozoa is of little 
or no importance. It is to be remarked in this 
connection, however, that the spermatozoa resist 
disintegration to a remarkable degree, and may 
be discovered in the urine entire for several days 
after its elimination. 

Albumen is a constituent of the seminal fluid ? 
therefore, when the latter is present to any con- 
siderable extent in the urine, it is possible to get 
tests for albumen. It is sufficient simply to warn 
against such a source of error. 

Fungi. 

The fungi which may be found in urinary sedi- 
ments consist of the saccharomyces, sarcinae, and 
bacteria. 

Saccharornyces. — Peneilium glaucum (or acid 
fermentation spore, as it is called by many who 
believe that it plays a part in the changes of that 
stage) is found in acid urine as small oval spores 
united in chains which branch here and there, 
forming characteristic thalli. Growth is by bud- 
ding. Practically, the importance of the Peneil- 
ium is the liability of the observer to confound 



OF THE URINE. 123 

it with the oval form of calcic oxalate, abnormal 
blood disks, and the sugar spore. Calcic oxalate 
crystals do not unite in chains, and are biconcave 
in appearance. The blood globule, although of 
about the same size, is not oval, and gives no evi- 
dence of budding. The sugar spore is larger. 

Torulce cerevisice, or sugar spores, are found in 
saccharine urine, or in urine which has been stand- 
ing in a vessel that previously contained sugar. 
In appearance they differ from the Pencilium only 
by the increased size of the individual spore, which 
is half as large again. 

The sarcina of vomitus has been encountered 
in the sediment a few times. It is composed of 
numerous spores arranged in cubes, four deep (or 
some multiple of four). Many attempts have 
failed to show that the form met with in the urine 
is an independent smaller variety originating in 
the bladder. It is probable, therefore, that when 
present in the urine the sarcina is extraneous, and 
not indicative of a pathological process. 

A great variety of bacteria may be found in 
urine, especially after it has undergone decompo- 
sition. There is reason to believe that at times 
bacteria exist in the urine when passed, but in the 
great majority of instances these organisms gain 
access only after the urine has been exposed to 
the air. The alkaline fermentation of the urine 



124 CLINICAL EXAMINATION 

is believed by many to be due to the decomposi- 
tion of urea by the action of a micrococcus which 
Cohn has called M. Ureae. It is probable that 
this organism is often introduced into the bladder 
by the passage of unclean catheters and sounds, 
the result of which is a bacterial fermentation in- 
side the bladder, and the conversion of the urea 
to amnionic carbonate. The innocuous acid urine 
thereby becomes changed to a fiery alkaline irri- 
tant, which may by its action upon the urinary 
tissues induce serious consequences, and even 
death. 

Other forms, such as the rod, vibrio, and lepto- 
thrix, may be encountered, either singly or massed 
together as zoogloea. 

When present in quantity, bacteria impart a 
cloudiness to the urine which, inasmuch as they 
pass the pores of the filter-paper, is not wholly 
removed by filtration. When present together 
with considerable mucus, the pores of the filter- 
paper become more or less plugged, and the urine 
is only difficultly filterable. Under such circum- 
stances the precipitation of the earthy or (if urine 
is already alkaline) alkaline phosphates will carry 
down the bacteria and mucus, after which the 
urine may be filtered with ease. 

In this connection it may be said that the Ba- 
cillus tuberculosis has occasionally been detected 



OF THE URINE. 125 

in the urine. When found, a considerable quantity 
of pus and disintegrated tissue is usually present 
as well. 

To detect the bacilli, allow the urine to stand 
for a short time, and place a little of the pus be- 
tween two cover-glasses. Dry each carefully, and 
stain like ordinary phthisical sputum. 

Morbid Growths. 

Cancer cells, or other evidences of morbid 
growths, are very seldom met with in the sedi- 
ment, for they do not pass out with the urine un- 
less mechanically dislodged by a catheter or other 
instrument. Even then they can be differentiated 
from the normal cells of the urinary passages 
only with the greatest difficulty. In short, no 
proof of neoplasm can be expected by an exam- 
ination of the sediment. 

Entozoa. 

The hooklets as well as the cysts of the echino- 
coccus have been discovered a few times in the 
urine; also the vermiform parasite Filaria sanguinis 
hominis, with which chyluria is associated. Neither 
is common in this climate. Other entozoa are too 
rare to be mentioned. 



126 CLINICAL EXAMINATION 

Extraneous Matter. 

This class includes a great variety of substances 
which may be met with in the examination of the 
sediment, and with which every student should 
familiarize himself. Among such are fibres of 
cotton, woollen, and linen ; human hair, cat's hair, 
splinters of wood, oil globules, air bubbles, and 
starch granules. Finally, if the slide be not thor-* 
oughly cleaned, the remains of a previous examina- 
tion, or scratches and marks on the slide, may 
mislead, or at least perplex, the beginner. 

To preserve Urinary Sediments for Subsequent 
Examination. 

Crystalline sediments are preserved only with 
difficulty, and inasmuch as they are so readily ob- 
tainable, there is no advantage in attempting their 
preservation. Organized sediment, on the other 
hand, may best be preserved in a filtered solution 
of acetate of potassium, to which a little phenol 
or salicylic acid has been added. The urine is 
separated from the sediment by decantation, and 
replaced by the potassium acetate solution after a 
few decantations with it. 



OF THE URINE. 127 



CHAPTER IV 



URINARY CONCRETIONS, 



Urinary concretions are hard, mineral-like bod- 
ies of varying size. They are at times voided in 
the urine, or, if too large to pass the urinary ducts, 
become lodged in some portion of the urinary pas- 
sages. In the latter case they may be situated at 
any point whatever, from the kidney tubules to the 
meatus ; in fact, they may be so fused as to form 
a more or less continuous stony cast of the whole 
urinary tract. 

They are limited in size only by the dimensions 
of the cavity or passage in which they lie. This 
property of size forms a ready basis for their 
classification, and concretions are therefore divided 
into sand, gravel, and calculi. 

Sand usually consists of small crystals, which are 
seen clearly only by the aid of a lens of low power. 

Grravel consists of larger crystals, which are easily 
seen with the unaided eye, and of such a size that 
they pass the urethra without difficulty. The con- 
tinual rubbing of the gravel particles on each other 
frequently results in " facetting " many of them. 



128 CLINICAL EXAMINATION 

Calculi are concretions which are too large to be 
spontaneously voided. 

The color of a concretion varies according to its 
composition, and whether it has been acted upon by 
blood pigment, — white, yellow, or brown. 

The rationale of concretion formation is very sim- 
ple. Any change occurring in the urine, while yet 
within the body, whereby the soluble constituents be- 
come insoluble, is followed by a separation of those 
substances, either in a crystalline or amorphous con- 
dition. The irritation of the epithelium, induced by 
the passage of the insoluble matter, causes an in- 
creased secretion of mucus, by which the precipi- 
tated matter becomes agglutinated, and the masses 
thus formed serve as nuclei of future calculi. 

It has already been shown, in speaking of the 
processes of urine fermentation, how the various 
non-organized constituents of the urine are ren- 
dered insoluble. It follows, therefore, that the same 
causes which bring about those changes are equally 
causative of concretions and calculi ; viz. increased 
acidity of the urine, however induced, is followed 
by a separation of the acid urates and uric acid, 
and increased alkalinity by the precipitation of the 
earthy phosphates (amorphous when precipitated by 
fixed hydrates, crystalline when due to fermentative 
processes). Any increased formation, as following 
upon defective oxidation of the less soluble normal 



OF THE URINE. 129 

or abnormal constituents, and finally the presence 
in the passages of foreign particles (bit of catheter, 
wood, etc. in the bladder) may be a cause of calcu- 
lus. The presence of any foreign body (including 
a calculus) in the bladder excites an inflammation of 
that viscus, which results at the time in an alkaline 
urine with a deposition of the phosphates, and later 
in hypertrophy, dilatation, and ulceration of the 
bladder walls, with the consequences arising there- 
from. It is due to these spontaneous changes that 
a distinction has arisen between primary and 
secondary portions of a calculus. Those portions 
which are first to form are accordingly called 
primary, while those which are formed as a result 
of the changes induced by the presence of the pri- 
mary portions are called secondary. 

The constituents of the primary and secondary 
portions are tabulated as follows : — 

Primary. Secondary. 

Uric acid. Urate of ammonium. 

Urates. Earthy phosphates. 

Calcic oxalate. Calcic carbonate. 

Calcic phosphate. ( Not common in 
Calcic carbonate, i human urine. 
Cystine. 
Xanthine. 
Indigo. 
Urostealith. 
Silica. 
Bilirubin. 
Blood-clot. 

Albuminous substances. 
Foreign bodies introduced into the bladder. 

9 



130 CLINICAL EXAMINATION 

In connection with the above distinctions, a cal- 
culus is also divided into a nucleus, body, and crust. 
The nucleus and body usually consist of the pri- 
mary constituents, while the crust is deposited as a 
result of the alkaline changes of the urine, and 
therefore consists of secondary portions. 

The surface of a calculus may be smooth or 
rough. Smooth calculi always attain a larger size 
than rough ; hence calculi of uric acid and phos- 
phates are frequently of considerable size. Calculi 
of calcic oxalate always have a rough surface, and 
on that account are often called mulberry calculi. 
They are productive of greater irritation, and in- 
duce secondary changes sooner than the smoother 
and hence less irritating varieties. 

A calculus grows by the deposition of successive 
layers about the nucleus. This frequently occurs 
irregularly, as shown by the position of the nucleus, 
which may be either at the centre or at some point 
nearer the periphery. 

Calculi are not always of simple composition, but 
oftener compound, i. e. composed of different con- 
stituents, which are frequently arranged in concen- 
tric lamellae. Thus a history of the growth of the 
calculus may be obtained by an analysis of its 
different layers. 

The number of calculi varies. As many as one 
hundred have been counted in one cavity. In such 



OF THE URINE. 131 

eases the rubbing of one calculus on another may 
give rise to many modifications in shape, — round, 
oval, irregularly oval, facetted, etc. Sometimes two 
nuclei become united, and subsequently covered 
with a secondary deposit. 

The Examination of a Calculus. — The calculus is 
first sawed in two, and with a penknife a little of 
each layer in succession is scraped off into a watch- 
glass and examined. 

The first step is to determine the presence of 
uric acid, and the second, whether it is free or com- 
bined as urates. The following scheme may be 
useful as a guide to the determination of the ordi- 
nary constituents of calculi. 

ANALYSIS OF URINARY CALCULI. 
(1.) Preliminary Examination. 

Heat scrapings on platinum : — 

Albumen = flame c odor of burnt horn. 

Urostealith = flame c odor of shellac and benzoin. 

Cystine = flame blue, odor of S0 2 . 

Xanthine and Uric Acid = no flame, — char. 

Alk. Urates = alk. residue sol. in H 2 0. 

Earthy Phosphates = residue sol. in HA s effervescence. 

CaO -f- CaC0 3 = residue sol. in HA c effervescence. 

CaC0 3 — original powder sol. in HA c effervescence. 

CaO — original powder insol. in HA. 

Silica = residue insol. in HC1. 
Murexide Test for H 2 U : — 

HN0 3 + evap. = pink residue -f NH 4 OH = purple color = Uric 
Acid and Urates. 

HNO3 + evap. + KOH = violet disappears on heat, if H 2 U. 

Violet increases on heat, if Xanthine. 



132 CLINICAL EXAMINATION 

(2.) Systematic Examination. 

Presence of uric acid shown by (1). Boil scrapings in H 2 and 
filter. 

A. Filtrate + HC1. Let stand 24° = crystals H 2 U. 
Bases in sol. Concentrate. 

CatJ = 1 gtt + (NH 4 ) 2 = cryst. CaO. 

MgU = 1 gtt + NH 4 OH + Na 2 HP0 4 = cryst. MgNH 4 P0 4 . 

Na 2 U = 1 gtt + PtCl 4 = after cone, prisms, Na 2 PtCl 6 . 

K 2 Uand (NH 4 ) 9 U = 1 gtt + PtCl 4 = DodecahedraJ K 2 PtC1 6- 

4 '- 'l(NH 4 ) 2 PtCl 6 . 

K 2 U evap. and ignite on mica. Res. + HC1 + PtCl 4 = K 2 PtCl 6 . 

(NH 4 ) 2 U evap. and ignite, no cryst. c PtCl 4 . 

B. Portion insol. in H 2 + HC1. 
H 2 U == insol. 

CaC0 3 = sol. c effervescence. Filter + NH 4 OH = ppt. 

CaO, Ca 3 (P0 4 ) 2 and MgNH 4 P0 4 . 
Wash CaO insol. in HA Filter + (NH 4 ) 2 6 to filtrate. 
Ca 3 (P0 4 ) 2 gives ppt of CaO. Filter + NH 4 OH to filtrate = 
ppt MgNH 4 P0 4 



OF THE URINE. 133 



CHAPTER 7. 

THE URINE AS AFFECTED BY GENERAL DISEASES. 

The urinary excretion bears an intimate rela- 
tion to the various metabolic processes. This is 
shown by the fact, that, in many constitutional dis- 
eases, modifications of the excretion are so con- 
stant that a systematic examination of the urine 
becomes at times of decided value in diagnosis. 

In the first place, variation in the quantity of 
urine passed, e. g. such symptoms as polyuria, 
oliguria, and anuria, is characteristic of several 
general affections, as follows. 

Polyuria, or the passage of a large amount of 
urine, is characteristic of the two forms of diabetes 
and hydruria, whose specific characters have al- 
ready been stated (vide page 13). In addition, it 
may be said that, aside from excessive drinking, 
hydruria is frequently the result of severe mental 
disturbances, e. g. great anxiety, grief, nervousness, 
etc., or of apoplectic hemorrhages. In the latter 
instance, the increased flow begins about half an 
hour after the attack, and in severe cases there 
may be an associated albuminuria and glycosuria. 



134 CLINICAL EXAMINATION 

Such cases warrant a grave prognosis. Ordinary 
hydruria ceases in a few days. 

Polyuria is also usual in convalescence from 
most acute diseases, and quite characteristic of 
certain forms of renal disease. 

Oliguria, or diminished urine, characterizes the 
active stage of most acute febrile processes, and 
many chronic diseases. In fact, slight oliguria 
occurs in all chronic diseases except the two forms 
of diabetes. 

It is a matter of some consequence to the healthy 
individual if he persistently fails to pass a full 
litre of urine daily. The urine becomes concen- 
trated, and, aside from acting as an irritant to the 
renal tissues, there is also danger of developing 
a calculus diathesis, i. e. a tendency to the separa- 
tion, in the urinary tract, of the less soluble con- 
stituents of the urine. This tendency can in most 
cases be corrected by drinking more water. 

Anuria, or suppression of the urine, is a serious 
condition, and arises from two general causes : — 

1. A mechanical obstruction to the flow, situated 
somewhere between the meatus and renal pelves. 
Most frequently this form is due to the impaction 
of a stone in the ureter of a person having (a) but 
a single functional kidney, or (6) some malforma- 
tion whereby only one ureter exists. It occurs 
next in order of frequency as a result of the destruc- 



OF THE URINE. 135 

tion or stenosis of the terminal ends of the ureters 
by morbid growths at the base of the bladder. Of 
course oliguria precedes the anuria in such cases. 
Finally, stenosis anywhere in the course of the 
urethra, the impaction of calculi in the urethra, 
or the obstruction (by bits of neoplasm, ropy urine, 
etc.) of the urethra at its point of union with the 
bladder, may give rise to a temporary anuria. 

In unrelieved cases, retention, dilatation of the 
channels behind the point of obstruction, hydro- 
nephrosis, and cystic dilatation of the kidneys en- 
sue, culminating in uremic convulsions and death. 
Such cases of anuria are to be considered as 
obstructive. 

The urine, for it is rare that a little is not voided 
before death occurs, is pale, at times slightly tinged 
with blood, watery, and of very low specific gravity. 

2. Organic disease of the renal tissue, whereby it 
is no longer able to separate the urine from the 
blood. This condition obtains just before the fatal 
termination of renal diseases. In this class are to 
be included also those cases which are apparently 
due to some disturbance of innervation, whereby 
the separation of the urine is temporarily sus- 
pended. Such forms of anuria are met with in 
severe poisoning by turpentine and other irritants, 
in states of collapse or shock, after catheterization, 
etc. They form a group quite opposed to the 



136 CLINICAL EXAMINATION 

former in cause, duration, and termination, and 
may be considered as non-obstructive. 

The urine of these cases is high-colored, concen- 
trated, albuminous, and contains casts. 

Cases of non-obstructive anuria are seldom fatal, 
last only a day or two, and are in most cases easily 
relieved. Cases of obstructive anuria are nearly 
always fatal, run a longer course, a week or ten 
days, and are beyond means of relief. 

After the above, the modifications of the urine 
to be observed are those which are dependent on 
the nature of the process, viz. whether febrile or 
not, and, in the same connection, whether acute or 
chronic. 

Fever urine is diminished in amount, high-colored, 
of increased acidity and specific gravity, and con- 
tains considerable sediment. As a result of the 
concentration, the total solids are relatively and in 
some cases absolutely increased. Urea and uric 
acid are both increased, and in the same propor- 
tion ; but in those cases in which respiration is hin- 
dered, uric acid is increased in a greater propor- 
tion than urea. If the case is about to terminate 
fatally, the amount of urea decreases. If the 
temperature is high, there may be albuminuria. 
If the fever is accompanied by any considerable 
exudation, e. g, pneumonia, peritonitis, etc., the 
chlorides disappear from the urine. In ordinary 



OF THE URINE. 137 

febrile conditions the absolute amount of chlo- 
rides is diminished; but, owing to the diminished 
quantity of urine, they may be relatively normal. 
Absorption of the exudation is followed by the 
reappearance or increase of the chlorides. 

With convalescence, the concentration of the 
urine gradually disappears, the reaction becomes 
more nearly neutral, the specific gravity falls? and 
the amount increases. The increase may consider- 
ably exceed the normal (2000 c. c), but as health 
is re-established the quantity again diminishes, and 
becomes settled at the normal point. 

The urine of intermittent fever is an exception to 
the ordinary rule. In this affection, the urine is 
usually normal on the day of the paroxysm, and 
exhibits febrile characters the day after. 

By an examination of the urine alone, no differ- 
ence can be determined between the febrile urine 
and that due to simple, non-febrile concentration. 

Besides these general characters, the urines of 
acute febrile diseases are often peculiar in some 
special way, as follows. 

In peritonitis the chlorides are frequently ab- 
sent, and the incloxyl much increased. 

In rheumatic fever the chlorides follow the gen- 
eral rule, and the phosphates are usually increased. 
If the rheumatism becomes complicated with peri- 
carditis, the chlorides and earthy phosphates will 
disappear. 



138 CLINICAL EXAMINATION 

The differential diagnosis between typhoid fever 
and meningitis is often extremely difficult, but 
may at times be greatly facilitated by a careful 
consideration of the urine, viz. : — 

Typhoid Fever. Meningitis. 

In early stage excessively acid. Only slightly acid at first. 

Sp. gr only slightly increased. Sp. gr. considerably increased. 

Chlorides normal or slightly di- Chlorides much diminished, 
minished. 

Phosphates diminished. Phosphates much increased. 

Boiling of urine in a test 
tube is sufficient to precipi- 
tate the phosphates. 

Of late, the so-called diazo-reaction has been 
used to confirm the existence of the typhoidal 
state. This reaction, however, is not observed in 
all cases of undoubted typhoid, and it does occur 
in other affections, viz. tuberculosis, measles (de- 
squamative stage), and in albuminous urines asso- 
ciated with extreme pyrexia. The reaction may 
be obtained from the urine at about the end of 
the first week, and coincident in time with the 
appearance of rose-spots on the body. 

Two solutions are required : — 

Solution A. 

Hydrochloric acid v\ 72, or 1 part. 
Sulphanilic acid gr. 10, or to saturation. 

Distilled water 5 3, or 20 parts. 



OF THE URINE. 139 

Solution B. 
\% solution (freshly prepared) Sodic Nitrite in distilled water. 

To perform the test : — 

In a test tube put of Sol. A 25 parts. 

Sol. B 1 part. 

Urine 26 parts. 

Amnionic Hydrate to alkalinity. 
Positive result = an immediate brilliant crimson red color and a 
greenish yellow precipitate in 24°. 

Acute yellow atrophy of the liver, typhus fever, 
small-pox, and poisoning by arseniuretted hydro- 
gen and phosphorus, are not characterized by an 
increase, but on the other hand by a great dim- 
inution, if not entire absence, of urea. As a re- 
sult of the morbid processes, complete oxidation 
of the nitrogenous tissues does not occur, and in 
the place of urea and uric acid, leucine and tyrosine 
are excreted. Albuminuria and hemoglobinuria 
are also observed in these cases. 

Acute intestinal diseases are accompanied by an 
increase of indoxyl (e. g. 98 milligrams), but only 
in case it is the small intestine that is affected. 

During the acute stage of cholera, the amount 
of urine, as well as of urea, is diminished. Much 
of the latter is eliminated in the sweat and faeces. 
Indoxyl, however, is increased. During conva- 
lescence the urea and amount of urine increase 
in about the same proportion. 



140 CLINICAL EXAMINATION 

In yellow-fever the urea is not so much in- 
creased as in ordinary cases of fever. 

The urine of chronic disease exhibits characters 
incident to the decreased metabolic activity of the 
body. The amount of urine is somewhat dimin- 
ished ; the solids are also diminished more or less, 
in proportion to the impaired appetite. Usually, a 
secondary affection of the kidney, as shown by 
albuminuria, is present as well. In the majority 
of cases, the urine is pale and feebly acid, but 
there are many exceptions. 

In chronic diseases of the liver, the urine is high- 
colored, excessively acid, diminished in quantity, 
and of high specific gravity. The absolute amount 
of total solids, however, is diminished, and the 
diminution of urea is in direct proportion to the 
extent of the hepatic destruction. There is usu- 
ally an abundant sediment of urates and calcic 
oxalate. The coloring matters are relatively,* and 
the indoxyl absolutely increased. As a rule, phos- 
phoric acid is diminished. 

In chronic rheumatism, the urine is apt to re- 
semble that of acute disease. It is high-colored, 
excessively acid, and contains an increase of urea. 
Otherwise, the solids are diminished. Calcic oxa- 
late is generally present in the sediment. 

In chronic gout, the uric acid is diminished dur- 
ing a paroxysm, but during the intermission it is 
increased. 



OF THE URINE. 141 

In chronic diseases of the spine, the indoxyl and 
phosphates are increased. 

In chronic diseases of the bones, the phosphates, 
especially the earthy phosphates, are increased. 

In leukocythaemia the proportion of uric acid to 
urea is increased. The latter may or may not be 
diminished. In many cases there are concomitant 
fatty changes in the kidneys, as evinced by albumi- 
nuria, fatty epithelium, and fatty casts. 

In chlorosis and anaemia, as a result of the di- 
minished tissue metamorphosis, the urine is pale. 
The urea and uric acid are diminished, usually in 
proportion to the destruction of red globules. 

In Addison's disease the urea is diminished and 
the indoxyl increased. 

In scurvy and purpura hemorrhagica, as a result 
of the destruction of the red-blood globules, hemo- 
globinuria frequently occurs, and from an asso- 
ciated parenchymatous nephritis there is albumi- 
nuria, and in the sediment casts are found. 

In phthisis, the urine follows the febrile type ; 
it is high-colored, but the specific gravity is not 
especially raised. The solids are diminished, ex- 
cept the earthy phosphates, which are increased 
in proportion to the destruction of lung tissue. As 
a result of the impeded oxidative processes, uric 
acid is apt to be increased. There may also ex- 
ist a secondary kidney affection, not unlike active 
hyperemia. 



142 CLINICAL EXAMINATION 

In chronic organic disease of the heart, the urine 
is apt to be febrile in character. Both urea and 
uric acid are relatively increased. The urea is 
absolutely diminished, whereas the uric acid may 
be absolutely increased. In addition, a slight al- 
buminuria exists, and in the sediment are found a 
few casts, — passive hyperemia. 

Following the general rule of effusions and exu- 
dations, the chlorides will be diminished in cases 
of dropsy ; but when once absorption of the effusion 
takes place, they will increase to normal. With 
the increase of the dropsy, the urea increases and 
the urine becomes febrile in character ; but as ab- 
sorption occurs, there is an absolute increase of the 
normal solids. 

In all dropsical cases there is usually some asso- 
ciated renal affection. 

Extensive disease of the skin is usually accom- 
panied by renal disturbances. In some cases the 
sulphates appear to be increased. 

In cases of melanotic cancer, the urine is usu- 
ally normal in color when passed, but on standing 
turns dark brown or black. This is probably due 
to the oxidation of some chromogenous substance 
as yet unknown. When the growth is increasing 
rapidly, this color change is not so frequently 
observed. 

In cases of malignant disease affecting the ab- 



OF THE URINE. 143 

dominal viscera, the urine is febrile in character. 
The urea and solids are, however, much dimin- 
ished absolutely. Indoxyl is considerably in- 
creased as a rule. As in all cases of impaired 
oxidation, there is an abundance of urates and 
calcic oxalate in the sediment, and frequently some 
renal complication. 



144 CLINICAL EXAMINATION 



CHAPTER VI. 

THE URINE AS AFFECTED BY LOCAL DISEASES. 

When the urinary tissues, upon whose anatomi- 
cal integrity and physiological health the elimina- 
tion of normal urine depends, become diseased, an 
examination of the urine furnishes the most valu- 
able indications concerning the nature and location 
of that disease. 

The changes which are due to pathological pro- 
cesses may be confined on the one hand to the 
kidney itself, or on the other to some portion of 
the urinary tract below the kidney. Finally, both 
the kidney and the urinary tract below it may 
be affected simultaneously, although the extent 
and severity of the pathological processes may be 
greater in the one than in the other. 

Disturbances confined to the Kidneys. 

The evidences of renal disturbance are in the 
first place albuminuria; in the second, modifica- 
tions in the physical and chemical characters of the 
urine ; and finally, the presence in the sediment of 
tissue-elements and casts which are suggestive of 
renal disintegration. 



OF THE URINE. 145 

In a general way, it may be said that in each of 
the renal diseases these evidences are associated in 
a more or less typical way, and it is by the correct 
interpretation of this association that a diagnosis 
of each affection is made. Before passing on to a 
detailed description of these evidences as they 
occur in the different forms of kidney disease, it 
may be well to consider briefly some facts con- 
nected with the etiology and pathology of nephritis 
in general. 

The intimate relation which has been shown to 
exist between the blood and the kidney finds ex- 
pression, on the one hand, in the kidney alterations 
to which disease of the blood gives rise, and, on the 
other, in the changes of the blood and vascular 
apparatus which are produced by disease of the kid- 
ney. Since the kidneys not only separate the water 
from the blood, but also the solid products of retro- 
grade metamorphosis, it is quite conceivable that 
any alteration of the latter, either in quantity or 
quality, will have a marked influence on the renal 
tissues. Then, again, it is clear that any essential 
disturbance, either functional or structural, of an 
organ so important in removing from the body the 
water and excrementitious matter, may bring about 
an alteration of the vascular constituents. 

The first of these propositions (blood composi- 
tion) is important, since it explains why it is that 

10 



146 CLINICAL EXAMINATION 

renal complications are so frequently associated 
with or succeed general disturbances, the so-called 
nephritides due to "humors in the blood." Con- 
spicuous among these are the nephritides of infec- 
tious disease. In scarlet-fever and diphtheria, for 
example, secondary renal troubles are so constant 
that they almost form a part of the picture of those 
diseases. In typhoid fever, recurrent fever, and 
fibrinous pneumonia, the kidney changes are not 
so constant, but do occur with such frequency that 
they may be regarded as possible complications. 
Not only in acute, but in chronic diseases, malaria 
and syphilis, secondary kidney changes occur. 

With respect to the pathogenesis of these sec- 
ondary complications, it is not always evident that 
the specific irritant is to be found in the kidney. 
In certain cases, e. g. embolic nephritis of ulcera- 
tive endocarditis, this would appear to be the case. 
In other cases, e. g. nephritis occurring at the end 
of acute fibrinous pneumonia, in which Nauwerck 
has proved the presence in the kidney of the cap- 
sule coccus, it may be probable. But in the most 
frequent form of infectious nephritis (scarlet-fever) 
no such evidence exists. Hence, in most cases it is 
probable that the nephritis is not so much due to 
the presence of the infectious agent in the kidney 
as to the action of some deleterious substance 
(ptomaine) developed in the course of the infection 



OF THE URINE. 147 

which the kidney is eliminating from the blood. On 
the other hand, severe nutritive disturbances, which 
are developed in the course of chronic infectious 
diseases, may be the cause of secondary renal dis- 
ease, e. g. the amyloid degeneration associated with 
pulmonary tuberculosis and syphilis. 

Although the above cases are all secondary, yet 
there are many instances of nephritis which are 
undoubtedly primary. The nephritides due to ex- 
posure to wet and cold, or other indefinite cause, 
are examples of this class. Even here the cause 
may be an infectious one, which is localized in the 
kidney, or it may be a general toxaemia, the expres- 
sion of which is local. 

It is undoubtedly proved that many poisons which 
are coursing in the blood may be carried to the kid- 
neys, and there give rise to extensive alterations. 
In some of these toxic nephritides the alterations 
in the kidney appear to be due to the direct, in oth- 
ers to the indirect, action of the poison in question. 
Thus, cantharides, turpentine, and chromic acid are 
directly harmful to the kidney tissue with which 
they come in contact, whereas it is probable that 
some other poisons do harm through the action of 
a decomposition product which is developed as a 
result of their presence in the body. The kidney 
changes associated with an intravascular destruction 
of red corpuscles (severe burns) is a case in point. 



148 CLINICAL EXAMINATION 

In certain chronic renal affections a similar cause 
(the presence of deleterious substances in the blood) 
seems not improbable. These substances may in 
some cases be derived from without, e. g. alcohol ; 
and in others from within, e.g. the products of 
retrograde metamorphosis. 

No sharp line between the various etiological 
factors can be drawn, and in many instances 
chronic renal disease fails of any satisfactory ex- 
planation. 

Whether clue to infectious, toxic, or unknown 
causes, the pathological alterations of the kidney 
are of two general types, according to the nature of 
the process, on the one hand, and to its situation in 
the renal tissue, on the other. 

Among the former, disturbances of circulation, 
inflammation, and degeneration are to be included ; 
and among the latter, changes which may be seated 
in the glomeruli, epithelium, or vascular and inter- 
stitial tissue. 

Disturbances of circulation consist either in an 
increased amount of blood in the organ (hypere- 
mia), or in a diminution of the same (anemia). 
Anaemia as an independent affection of the kidney 
is probably never more than temporary, and is un- 
accompanied by definite alterations in the urine. 
Further consideration of this condition is therefore 
unnecessary. Hyperemia, on the other hand, has 



OF THE URINE. 149 

been found to be a tolerably frequent condition, and 
accompanied usually by more or less definite signs. 
The increased amount of blood in the organ may be 
due either to an increased afflux, or to a diminished 
efflux. The former condition, because due to causes 
directly operative in dilating the vascular channels 
of the kidney, is called active hyperemia, whereas 
the latter, because due to causes preventing the 
usual outflow of blood from the organ, is called 
passive hyperaemia or passive congestion. 

Hyperemia is one of the essential features of 
every acute inflammation ; hence it happens that 
every inflammation of the kidney must have passed 
through the stage of active hyperemia. Not only 
this, but the condition of hyperaemia persists so 
long as the inflammation is active, and differs only 
in degree. The same causes, then, which produce 
a nephritis, are when less severe causative of active 
hyperaemia. It follows that the point at which a 
severe hyperaemia becomes a mild but true inflam- 
mation (nephritis) is often quite indefinite, and a 
diagnosis based on an examination of the urine 
alone must in such cases be equally uncertain. 

Besides the hyperaemia, which may be so severe 
as to cause rupture of the vessels (hemorrhage), 
inflammation of the kidneys is also accompanied 
by round-cell exudation and secondarily degenera- 
tive changes. The exudation affects chiefly the 



150 CLINICAL EXAMINATION 

interstitial tissue and vessel walls, whereas the 
degeneration is confined almost wholly to the 
epithelium. 

Although inflammatory processes may bring 
about secondary degenerative change, it is equally 
true that degenerative change may in the end lead 
to inflammation. In either case, the inflammatory 
process is limited, as above suggested, to the vas- 
cular and interstitial tissue, and the degenerative 
process to the epithelium. In this connection, the 
fatty kidney due to phosphorus poisoning, severe 
general anaemia, and cholera, i. e. disturbances 
of nutrition, are to be distinguished from true 
inflammations. 

Upon such grounds as have been suggested, a 
classification of kidney inflammations has been 
made ; viz. parenchymatous, or those in which the 
epithelium is affected, and interstitial, in which the 
pathological processes are confined to the renal 
stroma and blood-vessels. Such a classification is, 
however, purely empirical; first, because in the par 
enchymatous class there is a degeneration and not 
an inflammation of the secreting cells, although 
an inflammation of the stroma may coexist; and 
secondly, because it is rare that an interstitial in- 
flammation is not accompanied or followed by some 
parenchymatous change. Finally, although the 
classification includes parenchymatous degenera- 



OF THE URINE. 151 

tions, it does not include a degeneration of the vas- 
cular and interstitial tissue, i. e. Amyloid. 

Hence the anatomical classification is not wholly 
satisfactory ; but inasmuch as it is the one generally 
adopted and best understood, it will suffice here. 

In the following descriptions of the urine as it 
varies in the different renal diseases, so much of 
the etiology and pathology has been introduced as, 
it is hoped, will serve to make the character of the 
urine more readily understood. 

Active Hyperemia (catarrhal nephritis, par- 
enchymatous degeneration, " cloudy swelling ") is 
simply an acute congestion of the kidney due to 
some slight irritation, and when uncomplicated and 
without permanent cause is only a temporary affec- 
tion, disappearing completely within a few days. 

Among the causes of active hyperemia are the 
presence in the urine of any irritant, either chemi- 
cal or zymotic ; the long continued elimination of 
concentrated urine, or urine containing bile pigment 
or concretions ; any cause whereby the kidney is 
overworked, e. g. chronic lung diseases and im- 
paired action of the skin ; intestinal disturbances ; 
and extension to the kidney of an irritation or in- 
flammation present in the lower membranes, — 
pelvis or bladder. 

The Characters of the Urine. — These vary some- 
what with the cause ; e. g. if the active hyperemia 



152 CLINICAL EXAMINATION 

is clue to some acute febrile disease, the peculiarities 
of febrile urine are observed, viz. high color, in- 
creased specific gravity, etc., with or without dim- 
inution of the chlorides ; if due to chronic disease, 
the urine is pale in color, of diminished specific 
gravity, etc. ; if due to concretions, particles will 
be found in the sediment. In the majority of in- 
stances, however, the urine is concentrated and of 
high specific gravity, but this is not essential to the 
diagnosis. More positive features are the presence 
of a slight trace of albumen, and in the sediment 
more or less free blood, an excess of renal cells 
frequently brownish in color, a few pure hyaline 
and fine granular casts, to which blood globules and 
renal cells may be adherent, and finally occasional 
blood and epithelial casts. 

In severer cases the albumen may be increased 
in amount, i. e. | to \ of 1%, as well as the number 
of casts, which may include those of the brown 
granular and fibrinous variety. Under such cir- 
cumstances, it cannot be positively affirmed, by the 
examination of a single specimen, whether it is a 
case of active hyperemia or acute nephritis. If it 
is a simple active hyperemia, the excess of albu- 
men and casts rapidly disappears, and within a few 
days the ordinary characters of active hyperemia 
are established. 

When the exciting cause is persistent and the hy- 



OF THE URINE. 153 

peraemia becomes long continued, fatty changes of 
the epithelium are induced, and as a result fatty cells 
and fatty casts may be encountered in the sediment. 

If due to a severe attack of fever, the hyperemia 
disappears with convalescence, and the quantity of 
urine for a time exceeds the normal. Under such 
circumstances, it may be difficult by an examina- 
tion of the urine to distinguish between a hyper- 
emia and a recovery from acute nephritis, since 
it differs from an acute nephritis, as has been said, 
only by the usually less extent and diminished in- 
tensity of the pathological process. 

Most cases terminate in recovery. 

Passive Hyperemia (chronic passive congestion, 
cyanotic induration) is characterized anatomically 
by a condition of venous stasis, affecting, accord- 
ing as the cause is local or general, one or both 
kidneys. The blood-vessels, especially on the ve- 
nous side, are markedly distended with blood ; the 
connective tissue, in which the vessels run, is in- 
creased in amount ; and at times the epithelium of 
the tubules undergoes more or less degeneration. 
Less arterial blood than usual flows through the 
kidneys, and the excess of blood which is present 
is largely venous in a more or less quiescent state. 
Under such conditions, a decreased flow of urine, 
a diminution of its solids, and the presence of al- 
bumen, become easily intelligible. 



154 CLINICAL EXAMINATION 

Causes. — The commonest causes of passive hy- 
peremia are pulmonary affections and uncompen- 
sated valvular diseases of the heart, in which the 
blood is prevented from passing through these or- 
gans in normal amount. The result is a general 
backing up of the venous blood in the right cavities 
of the heart, the great veins emptying into the right 
heart, and thence all through the body. The kid- 
neys therefore share the common fate. 

Among local causes are thrombosis of the as- 
cending vena cava above the point at which the 
renal veins enter it, or thrombosis of the renal 
veins themselves; and pressure, as by a tumor, — 
new growth, or in females a pregnant uterus, — 
upon these same venous trunks at some point in 
their course toward the heart. 

In pregnancy, the pressure is not so extensive as 
to cause an absolute decrease of the total solids, 
although the urine may be pale, and contain as 
much as i of 1% of albumen, together with hya- 
line and fine granular casts of large diameter. It 
cannot be positively affirmed that organic disease 
of the kidney exists, although such cases generally 
terminate in puerperal convulsions, followed by a 
genuine acute nephritis. 

Characters of the Urine. — In general, it is di- 
minished in amount; of high specific gravity (it 
may, however, be low) ; contains a slight trace of 



OF THE URINE. 155 

albumen ; there is an absolute diminution of solids, 
and a relative inerease of some (the urea and uric 
acid may be absolutely increased). The amount 
of chlorides will depend on the amount of effusion, 
as has elsewhere been explained. The sediment 
will contain hyaline and fine granular casts of 
small diameter, a virtual absence of blood and no 
excess of renal epithelium. 

Owing to the nature of its causes and its chronic 
course, passive hyperemia does not admit of a 
favorable prognosis, but by proper treatment, di- 
rected to the underlying causes, temporary im- 
provement may be obtained. 

Acute Parenchymatous Nephritis (acute dif- 
fuse nephritis, acute Bright's disease) is a true 
inflammation of the kidney. It may be due to long 
continued irritation (persistent active hyperemia), 
exposure to cold and wet, or it may be associated 
with many of the acute infectious diseases, notably 
scarlet-fever, diphtheria, measles, typhoid, typhus, 
recurrent, and yellow fevers, fibrinous pneumonia, 
septicaemia, and acute articular rheumatism. 

Anatomically the changes vary a great deal as 
to the particular region affected, their extent or 
diffusion, and the nature and severity of the cause. 
In many cases, e. g. scarlet-fever, only the glomer- 
uli appear to be affected. In these there is a swell- 
ing of the epithelium, granular infiltration of the 



156 CLINICAL EXAMINATION 

capillary wall, and exudation under the capsule 
of Bowman. Oftener, however, there is in acute 
nephritis more or less round-cell or hemorrhagic 
infiltration into the connective tissue and the space 
between the capsule of Bowman and the glomeru- 
lus. The epithelium of the uriniferous tubules 
undergoes granular degeneration (cloudy swelling) 
and subsequently becomes fatty degenerated. The 
lumen of the tubules is plugged with extravasated 
blood globules, desquamated epithelium, and solidi- 
fied albuminous material (casts). Physiologically, 
alterations in the nutrition of the tissues of the 
glomeruli, whereby their porosity or permeability 
is increased, is causative of albuminuria, and, as a 
result of inflammatory processes, both the pressure 
and rapidity of the blood stream in the glomeruli 
are diminished. 

It is quite clear that, in proportion to the extent 
and severity of the changes enumerated above, the 
urine will be albuminous, diminished in amount, 
colored (blood pigment), and laden with renal cells, 
blood corpuscles, and casts. As the disease pro- 
gresses, these characters vary, and, in accordance 
with that variation, acute nephritis may be divided 
into three stages. 

First Stage, — The amount of urine is consider- 
ably diminished, — 300-500 c.c. in 24°; dark brown 
or black in color, and usually acid in reaction. The 



OF THE URINE. 157 

specific gravity varies. In a general way it follows 
the quantity of urine. If the tubules are plugged 
to any great extent, it follows that the urine can- 
not get out ; hence the amount, as well as the solids, 
upon which the specific gravity depends, will be 
diminished together, and in about the same propor- 
tion. The specific gravity is also, to some extent, 
directly dependent on the amount of blood present. 
It may, therefore, be either high or low. The nor- 
mal solids are absolutely diminished. The amount 
of albumen varies with the severity of the disease 
and the amount of obstruction in the tubules. It 
is usually \ to 1|%. 

There is usually considerable brownish-colored 
sediment, the color being due to the free admix- 
ture of decomposed blood pigment. Upon exam- 
ination, the sediment is found to contain a large 
quantity of free abnormal blood-globules, and nu- 
merous brown granular renal cells ; also large 
numbers of blood, epithelial, brown granular, and 
fibrinous casts, together with an occasional pure 
hyaline and fine granular cast. 1 If the inflamma- 
tion is severe, pus corpuscles may be present. 

Second Stage. — As the disease progresses, fatty 
changes ensue, and in a few days fatty elements — 
fatty renal epithelium and fatty casts — make their 

1 Pure hyaline and fine granular casts are found in the sedi- 
ment of all the organic renal diseases. 



158 CLINICAL EXAMINATION 

appearance in the sediment, in addition to those 
elements already present. If the disease is to 
terminate fatally, the end comes during this stage ; 
if recovery be the issue (most usual), a change in 
the urine occurs, and this turning point is called 
" beginning convalescence." 

With the cessation of the inflammatory process, 
the blockade in the tubules is gradually raised ; the 
urine begins to flow more abundantly, and increases 
rapidly. Concomitantly, the absolute amount of 
solids begins to increase, the brown color gives way 
to a " smoky " hue, and the chlorides reappear. As 
the amount of urine increases, the albumen de- 
creases. There is a gradual, followed by a rapid, 
increase of the fatty elements, lasting one or two 
days. The brown granular and fibrinous casts 
decrease in number, and finally disappear ; the 
hyaline and fine granular still persist. During 
this " period of transition," a positive diagnosis 
from an examination of the urine cannot be made. 
As beginning convalescence merges into established 
convalescence, the urine changes again. 

Third Stage. — A reactional activity of the kid- 
neys sets in. The amount of urine transcends the 
normal daily figure, and may rise as high as 2500 
or 3000 c.c. The smoky color fades away, and 
the urine becomes pale. The solids, although rel- 
atively diminished, are now about normal. The 



OF THE URINE. 15 ( J 

albumen has become diminished to a trace. In 
the sediment may be found hyaline and fine gran- 
ular casts, an occasional blood cast, a few blood 
corpuscles and renal epithelial cells. The brown 
granular and fibrinous casts have entirely disap- 
peared, and the fatty elements have followed suit, 
although a few may be discoverable still. With 
complete return to health, the urine decreases to 
the normal amount, the amber color returns, the 
albumen and casts disappear, and, in a word, it 
becomes normal again. 

In acute nephritis, the return to health is not 
always progressive and uninterrupted. When con- 
valescence is apparently established, a careless and 
at times slight exposure will be followed by a 
renewal of the inflammatory processes. Such in- 
terruptions are termed " acute exacerbations." 
Abundant hemorrhage from the straight tubules 
occurs, in consequence of which the urine becomes 
blood-red (normal blood) in color. The amount 
of urine diminishes, and the albumen increases 
slightly. In this condition a resemblance to ac- 
tive hyperemia obtains. 

Dropsy, a common accompaniment of nephritis, 
is rarely observed in active hyperemia. 

Although unusual, several exacerbations may be 
directly causative of a chronic parenchymatous 
nephritis. 



1G0 CLINICAL EXAMINATION 

Chronic Parenchymatous Nephritis is rarely 
to be referred to a preceding acute nephritis ; 
oftener it is associated with chronic wasting dis- 
eases, which are accompanied by long continued 
suppuration. In general, the etiology coincides 
pretty closely with that of fatty degeneration. 
What the nature of the specific irritant may be 
is as yet undetermined. The progress of the dis- 
ease is gradual, and accompanied by no very ob- 
vious symptoms, to the patient until it has reached 
a considerable degree of development. Thus the 
chronic nature of this form of nephritis is defi- 
nitely established. Clinically, the patient suffers 
from digestive disturbances, lumbar pains, head- 
ache, and frequent micturition. He says that he 
is passing more water than usual, although this is 
to be attributed rather to the frequency with which 
he voids urine than to an absolute increase in the 
amount passed. Extreme pallor of the patient, 
and dropsy, are also striking symptoms. 

Anatomically, the kidneys undergo various 
changes. Fatty degeneration of the epithelium of 
the tubules and glomeruli is the characteristic and 
most constant alteration. At times there is, in 
addition, a true inflammatory condition, charac- 
terized by hemorrhages, round-cell exudation into 
the connective tissue, desquamation of the renal 
epithelium, and solidification of albuminoid ma- 



OF THE URINE. 161 

tcrial in the tubules. As in acute nephritis, there 
is a blockade of the eliminating channels, and 
a similar diminution in the amount of urine. 
In a few cases, if the interstitial tissue has been 
seriously involved, subsequent contraction of the 
kidney occurs, inducing in the urine all the char- 
acters of chronic interstitial nephritis. 

Following upon the changes above described, 
the characters of the urine will vary according to 
the activity of the disease, hence a distinction 
between the active and passive stages is to be 
observed. 

Character of the Urine. — Active Stage. — While 
the dropsy, which is invariably present, is increas- 
ing, the urine is high in color but not dark, dimin- 
ished in amount,— 500 to 800 c.c. in 24°, — and ex- 
ceedingly acid. The solids, with the exception of 
the chlorides (dropsy) and phosphates, are relatively 
increased in amount, but there is an absolute dim- 
inution of all, except perhaps uric acid. In this 
disease the albumen reaches the maximum limit, 
varying between J of 1% and 4 or 5%. 

The sediment is usually abundant, consisting 
chiefly of amorphous urates, due to the concentra- 
tion of the urine. In addition, there is a large 
number of fatty renal cells and compound granule 
cells. Fatty casts, often of large diameter, are nu- 
merous, as well as the pure hyaline and fine granu- 

ll 



162 CLINICAL EXAMINATION 

lar varieties. They may contain fragments of renal 
epithelium, and if the inflammation is conspicuously 
hemorrhagic they may be pigmented and contain 
blood globules, although this is more frequently 
dependent upon a coexistent active hyperemia. 

If the disease is to terminate fatally in this 
stage, numerous large waxy casts make their ap- 
pearance in the sediment. 

By proper treatment, the active symptoms may 
be checked, and the disease rendered less active ; 
in this case the character of the urine changes. 

Passive Stage. — If the dropsy is not increasing, 
and the patient is " holding his own," the amount 
of urine increases, — 1300 or 1400 c.c. in 24°. The 
solids likewise increase, but not to the normal 
standard. They are still absolutely as well as 
relatively diminished. The color becomes pale, 
and in fact the urine merely exhibits the usual 
characters of chronic disease. The albumen di- 
minishes somewhat. It may be \ of 1% more or 
less. There is still considerable sediment, and, 
with the exception of an excess of urates, is like 
that found in the active stage. 

The disease is not necessarily immediately fatal- 
After several years duration, atrophy of the renal 
tissue may occur. This fact leads many writers to 
speak of a third stage, in which the urine becomes 
almost identical with that accompanying chronic 



OF THE URIXE. 163 

interstitial nephritis. The essential points of dif- 
ference are, that (a) the amount of urine is not so 
much increased as in interstitial, and (5) if it is a 
urine of chronic parenchymatous nephritis, fatty 
elements are occasionally found in the sediment. 

Chronic Interstitial Nephritis is, like the pre- 
ceding, an affection of the kidneys, which develops 
slowly and insidiously, and frequently exists unde- 
tected until, months after the disease has become 
well developed, the patient is suddenly seized with 
a convulsion, which directs the attention of the phy- 
sician to the kidneys. 

The cause of the disease is as yet imperfectly 
understood. It is frequently found to be associated 
with gout, syphilis, and chronic lead poisoning, 
which suggest " chemico-toxic " influences. In 
many cases there is no sufficient cause to which the 
disease can be ascribed, and it must be regarded as 
idiopathic. Clinically, the patient suffers more or 
less from dyspepsia and headache, and, as the dis- 
ease becomes well established, there is a gradually 
increasing frequency of micturition, which at last 
compels the patient to rise once or twice during 
the night and pass his urine. There is also an 
associated hypertrophy of the left ventricle of the 
heart, which induces more or less palpitation. 
In uncomplicated cases there is, as a rule, no 
dropsy. 



164 CLINICAL EXAMINATION 

The anatomical changes consist of a gradual 
destruction of the kidney cortex, which is due to 
the contraction of the hyperplased connective 
tissue. The inflammatory infiltration involves at 
first isolated areas of the cortical connective tissue, 
blood-vessels, and neighboring glomeruli. Subse- 
quently, by contraction of the newly formed tissue, 
the surface of the kidney becomes markedly 
roughened or granular, corresponding to the areas 
of contraction. As the process extends, and the 
different islets of inflammation fuse together, the 
cortex becomes, after contraction, much reduced, 
and wellnigh obliterated. The kidney, as a whole, 
is reduced in size, may be to one fourth its original 
volume, and the granular appearance of its surface, 
alluded to above, has given to it the name of the 
small or contracted granular kidney. 

The epithelium of the tubules has, meanwhile, 
suffered degeneration and disintegration. Asso- 
ciated with the processes going on in the kidneys, 
there is a change in the blood-vessels. The failure 
on the part of the kidney to eliminate the urinary 
constituents, means, of course, their retention in 
the vessels. The irritation of the latter, to which 
such a retention gives rise, is manifested by a 
general arterial spasm, followed by arterio-fibro- 
sclerosis and consequent diminution of the vascular 
lumina. To meet this condition of affairs a com- 



OF THE URINE. 165 

pensatory hypertrophy of the heart ensues, which is 
a characteristic feature in all cases of well developed 
interstitial nephritis. 

The character of the urine depends directly upon 
these processes. In the early stages of the disease, 
when only isolated spots of the kidney are involved, 
little or no alteration of the urine is to be observed. 
By degrees, however, larger patches of tissue be- 
come affected, and many of the glomeruli and 
tubules are rendered useless for excretory purposes. 
The character of the urine gradually changes ; it 
becomes, not diminished, but — owing to the com- 
pensatory hypertrophy of the heart and the remain- 
ing glomeruli, which are functional — increased in 
amount. The power of the epithelium to excrete 
the solid constituents is impaired, and consequently 
the total solids suffer diminution. Albumen in 
small amount will be present, and, as the renal 
tissue contracts, a few cells may be rubbed off, and 
appear, together with a few casts, in the sediment. 

Character of the Urine. — In the early stages it 
varies slowly from the normal. The amount 
increases slowly ; at the same time the normal 
constituents show upon examination no marked 
change, perhaps only a slight diminution. A trace 
of albumen may be discoverable, and, after careful 
search, an occasional hyaline and fine granular 
cast. 



166 CLINICAL EXAMINATION 

In this stage, the clinical examination of a speci- 
men would hot differ, save in the amount of urine, 
from that observed in a case of passive hyper- 
emia. 

As the disease becomes more advanced, the urine 
becomes pale and is considerably increased (2000- 
4000 c.c.) in amount. The specific gravity, at the 
same time, decreases, — 1010 more or less ; 1005 
when far advanced. The normal solids are both 
relatively and absolutely diminished, with the ex- 
ception of indoxyl, which remains relatively nor- 
mal. This means, of course, an absolute increase, 
and interstitial nephritis is the only organic renal 
disease in which there is an absolute increase of 
indoxyl. The albumen measures \ of 1%, more or 
less. 

In the sediment, which is very slight, are hyaline 
and fine granular casts of small diameter (larger 
ones may be found in well advanced cases), and 
possibly an occasional renal cell. The sediment 
is so slight that it is necessary to let the urine 
stand several hours to insure settling of the casts ; 
and, furthermore, some care in the preparation of 
a slide will oftentimes be rewarded with a positive 
result, which might otherwise have been negative. 

When the kidneys have become so much atro- 
phied as to leave only six or twelve months of life, 
the urine again changes. The cardiac hypertrophy 



OF THE URINE. 167 

can no longer overcome the destructive obliteration 
of the glomeruli and tubules, and the amount of 
urine gradually falls to normal, and perhaps slightly 
below, — 1200-1300 c.c. In other respects, its char- 
acters remain unchanged, save that waxy casts may 
be found in the sediment. As a rule, the appear- 
ance of waxy casts is indicative of death within 
six or nine months. 

For a short time before death, the excretion of 
urine is markedly diminished, even to complete 
suppression. 

The disease is almost invariably fatal, and fre- 
quently prematurely so, from the rupture of athe- 
romatous cerebral vessels, which cannot withstand 
the increased cardiac activity. 

Amyloid Degeneration of the kidney is not an 
inflammation, but probably a nutritive disturbance, 
whereby a peculiar bacon-like substance possessed 
of definite chemical reactions (i. e. stains mahog- 
any-brown with iodine) makes its appearance in 
the cortex of the kidneys, affecting primarily the 
muscular coat of the afferent blood-vessels ; then, 
in succession, the glomeruli, vasa efferentia, and 
vessels of the pyramids. The vessel w r alls be- 
come thickened, and the lumen diminished. 

The causes of the amyloid change are not defi- 
nitely understood. It is observed, however, to be 
associated with chronic pulmonary consumption, 



168 CLINICAL EXAMINATION 

long continued wasting diseases, chronic suppura- 
tions (joint disease), and syphilis. The diagnosis 
is usually made from the clinical history, and the 
discovery of amyloid change in other organs, es- 
pecially in the liver and spleen. 

Character of the Urine. — Examined clinically, 
the urine is found to possess all the features which 
characterize interstitial nephritis, and is often quite 
indistinguishable from that of the latter disease. 
The essential difference, so far as the urine is con- 
cerned, is a higher specific gravity on the average, 
because it contains a more nearly normal quantity 
of solids. The albumen, too, is liable to be more 
abundant in amyloid degeneration. In the begin- 
ning, however, there may be none ; but as the 
degeneration progresses, the albumen appears, and 
gradually increases, even reaching 3%. The sedi- 
ment is the same as that found in chronic inter- 
stitial nephritis. 

It follows, therefore, that a quantitative estima- 
tion of the total solids is the only means whereby 
the urine of amyloid degeneration can be distin- 
guished from that of interstitial nephritis. 

Although the disease is incurable, the patient 
may live many years. 

The different varieties of organic renal disease 
have now been described in their uncomplicated 



OF THE URINE. 169 

form. More frequently, however, kidney diseases 
are combined with each other ; under these circum- 
stances, the diagnosis often becomes difficult and 
unsatisfactory. 

The more common combinations are : 

1. Chronic parenchymatous with interstitial ne- 
phritis (chronic diffuse nephritis). 

As it is unusual for chronic disease to exist inde- 
pendently of some interstitial change, it is quite 
unnecessary to diagnose by urinary examination 
chronic diffuse nephritis. The amount both of 
urine and of albumen will be governed by the dis- 
ease which predominates. For example, a nearly 
normal amount of urine containing | of 1 % of albu- 
men and fatty elements would suggest a predomi- 
nance of the parenchymatous process. As a rule, 
the course of chronic parenchymatous is more rapid 
than that of chronic interstitial nephritis. 

2. Chronic parenchymatous nephritis with amy- 
loid degeneration, the etiological factors of both 
these affections being very much the same. 

Chronic parenchymatous nephritis complicated 
with amyloid degeneration cannot, by an examina- 
tion of the urine, be distinguished from chronic 
diffuse nephritis. The detection of amyloid de- 
generation in the palpable viscera would render 
a diagnosis of amyloid complication in the kidney 
more probable. 



170 CLINICAL EXAMINATION 

In any combination, there may be a little acute 
nephritis superadded. 

3. Chronic parenchymatous with acute nephritis. 

In this case, the water is diminished in amount, 
the albumen increased, and in the sediment are 
found blood and fatty elements, also hyaline, blood, 
fatty, granular, and brown granular casts. By the 
examination of a single specimen it cannot be posi- 
tively affirmed whether it is the above combination 
or a case of acute nephritis in the second stage. 
If the former, the prognosis would be grave; if 
the latter, favorable. To establish the diagnosis, 
a history of symptoms covering a couple of weeks 
would be indicative of acute nephritis, whereas if 
chronic the symptoms would cover a considerably 
longer period. If, after repeated examinations, the 
fatty elements should presently disappear, it would 
be indicative of an acute nephritis, whereas the 
persistence of the fatty elements and a disappear- 
ance of the blood would prove the alternative. 
Finally, in this combination the amount of urine 
does not, as in convalescence from simple acute 
nephritis, exceed the normal. 

Senile Atrophy of the kidneys is, as its name 
implies, an affection of old age. It is a kind of 
slow interstitial nephritis. The changes, however, 
are not limited, as in interstitial nephritis, to the 
cortex, but involve both cortex and pyramids 



OF THE URINE. 171 

alike. The urine resembles that of passive hyper- 
emia, viz. diminished quantity, high colored, not 
markedly increased specific gravity, slight albu- 
minuria, and hyaline and fine granular casts in the 
sediment. 

Malignant Disease of the kidneys gives rise, as 
a rule, to no change in the urine, unless the cir- 
cumscribed irritation provokes a slight active hy- 
peremia. It is rare that any portion of the growth 
is detected in the urine. Infrequently, as a result 
of ulceration, pus and blood may be found. Other- 
wise, the diagnosis of malignant disease is quite 
impossible. 

Abscess of the Kidney. — In this affection, pus 
may be discharged into the tubules or renal pelvis. 
The character of the urine w T ill vary according to 
the nature and situation of the abscess. A diag- 
nosis cannot be made by an examination of the 
urine alone. 

Diseases of the Urinary Membranes below the 
Kidney proper. 

Pyelitis is an inflammation of the mucous mem- 
brane lining the renal pelvis. It is caused by the 
extension downward of inflammatory processes 
from the kidney (acute nephritis), or upward from 
the bladder, especially if the latter contains am- 
moniacal urine (cystitis). Irritating sediment or 



172 CLINICAL EXAMINATION 

concretions are also a frequent cause of pyelitis. 
The disease itself may be acute or chronic. 

Acute Pyelitis. — The urine is febrile in char- 
acter, acid in reaction, and, if concretions are 
present, excessively so. The sediment is usually 
abundant, and contains pus and blood, varying in 
amount, usually considerable, with the extent and 
severity of the affection. The per cent of albu- 
men varies with the amount of pus and blood 
present, — more in proportion to the quantity of 
blood, however, than to pus. During the early 
stages, cordate cells from the superficial layers of 
the pelvic mucous membrane, and, later, small 
round cells from the deeper layers, are present in 
the sediment. The presence of pus is quite char- 
acteristic of acute pyelitis. The pus corpuscles, 
mixed with blood globules and pelvic cells, are ar- 
ranged irregularly in clumps. At times they are 
aggregated into thick, short cylinders, suggesting 
casts from the papillary ducts. 

Not infrequently the inflammation extends to 
the straight tubules of the kidney, the evidence 
of which is the presence in the sediment of hy- 
aline, epithelial, and granular casts. (Compare 
Prostatitis, page 177.) It is not important, prac- 
tically, to differentiate between pyelitis and acute 
nephritis. 

When the pyelitis is caused by the irritating 



OF THE URINE. 173 

action of concretions, particles may be looked for 
in the urine. 

Chronic Pyelitis.— li the disease becomes chronic, 
the urine changes. It is pale (unless hemorrhage 
occurs), slightly acid, diminished in amount, and 
contains an abundant sediment, which settles 
slowly, not in flocculent masses, but as a thin film 
which adheres to the glass and is with difficulty 
picked up with the pipette. The sediment consists 
chiefly of pus in clumps, numerous small round 
cells from the deeper layers of the renal pelvis, 
and more or less blood; there is always a little. If 
concretions are the cause of the pyelitis, fragments 
are present in the sediment. On the other hand, 
there is usually no sedimentary evidence when the 
pelvic inflammation is due to local morbid growths 
and tuberculous processes. 

A calculus sufficiently large to obstruct the 
orifice of the ureter may cause a retention of urine 
in the renal pelvis. As the secretion of urine con- 
tinues, the pelvis gradually becomes distended, 
giving rise to the condition known as hydrone- 
phrosis ; or similarly, if the distention be largely 
due to pus, pyonephrosis. 

Ureteritis, or inflammation of one or both ure- 
ters, is a very rare disease. Inflammation which 
is extending either up or down the urinary mem- 
branes usually skips the ureters. The common 



174 CLINICAL EXAMINATION 

cause of ureteritis is the passage of concretions. 
In simple cases, the urine itself is unaffected, but 
the sediment may contain, besides bits of concre- 
tions, spindle-shaped cells from the tissues of the 
ureter, and, in addition, blood and pus. 

When there is a partial obstruction of the ure- 
ters, as may arise from the pressure of tumors, 
impacted concretions, and stricture of the urethra, 
the character of the urine is different. In such 
cases it is partially suppressed, — more or less 
anuria, — hence greatly diminished in amount. It 
is slightly albuminous, somewhat acid, and of low 
specific gravity. The solids are relatively and 
absolutely diminished. In the sediment may be 
found pus, blood, and cells from the seat of inflam- 
mation, and, after careful search, an occasional 
hyaline cast. This condition is, however, of rare 
occurrence. (Compare Anuria, page 134.) If the 
seat of obstruction is in the urethra, there usually 
is, in addition to the above, an inflammation of the 
bladder, or cystitis. 

Cystitis, as has already been intimated, fre- 
quently occurs from an extension of the inflam- 
matory process from the neighboring urinary tract, 
i. e. pyelitis or gonorrhoeal urethritis. In many in- 
stances the inflammation is apparently induced by 
the presence of foreign bodies in the bladder, — 
notably calculi. It is to be observed, however, 



OF THE URINE. 175 

that in such cases the cystitis is not so much 
dependent on the mere irritating influence of the 
stone as upon the introduction of unclean catheters 
and sounds used to determine its presence. Other 
cases of cystitis arise from stricture of the urethra, 
and paralysis of the vesicle sphincter. In the 
former instance there is a retention of urine in the 
bladder and an associated desire to micturate 
frequently. In the latter, there is a constant 
dribbling of urine. Under such conditions, the 
urethra contains a stagnating column of urine, 
and to this column the air, containing bacteria of 
decomposition, has direct access. As a result, the 
urine in the bladder soon becomes ammoniacal, and 
acts as a direct irritant upon the mucous membrane 
of the bladder. Finally, cystitis may be caused by 
the action of irritants eliminated in the urine (e. g. 
cantharides, certain foods, drinks, and infectious 
agents), or it may arise idiopathically, although 
very rarely, as a result of exposure to cold. 

According to its nature and activity cystitis may 
be acute or chronic. 

Acute Cystitis. — The quantity of urine is di- 
minished, concentrated, and more or less bloody. 
The solids are relatively increased, and the per 
cent of albumen varies, as in pyelitis, with the 
amount of pus and blood present. During the 
first few days of the disease the urine is acid, but 



176 CLINICAL EXAMINATION 

very soon the urea undergoes decomposition within 
the bladder, and the urine becomes alkaline. The 
ammonia, to which the alkalinity is due, gives to 
the urine its distinctly ammoniacal odor, which, 
if detected as it is voided, is quite pathognomonic 
of cystitis. 

A long continued acute cystitis may become 
chronic if the exciting cause persists, e. g. retention 
of vesicle calculi. 

Chronic Cystitis, — In untreated cases, the urine 
is pale, ammoniacal, of low specific gravity 
(usually), very turbid, and contains an abundant 
sediment ; frequently, if the amount of pus present 
is considerable, it is "ropy." The amount of albu- 
men will, as in the acute form, depend on. the pus 
and blood present. The sediment is only with 
some difficulty picked up by the pipette, and con- 
tains chiefly amorphous masses of bacteria, ammo- 
nium urate, triple phosphate, and disintegrated 
pus corpuscles. If the specimen examined is a 
fresh one, normal blood and bladder epithelial cells 
may be found in the sediment. To examine the 
sediment, the fluid urine should be decanted from 
the ropy mass and allowed to settle. 

In treated cases of chronic cystitis, the urine is 
not necessarily of alkaline reaction ; in fact, it 
is usually acid and not ropy. In the sediment- 
pus, blood, and bladder epithelium may be found. 



OF THE URINE. 177 

In other respects, the urine is the same as in un- 
treated cases. 

An inflammation limited to the neck of the 
bladder is a not infrequent complication of gon- 
orrhoea. In such cases, the urine is not alkaline, 
but acid. The sediment consists of blood and pus, 
together with an excess of cells from the neck of 
the bladder. There is no excess of bladder epithe- 
lium. Albumen in proportion to the amount of 
blood, usually only a trace, may be present. 

Prostatitis, or inflammation of the prostatic por- 
tion of the urethra, may arise, like the preceding, 
from the upward extension of a gonorrhoea. It is 
also frequently caused by the passage of calculi, 
and in connection with a stricture of the urethra. 
An abscess of the prostate gland may discharge 
into the urethra, with evidences of a prostatitis. 

The character of the urine is identical with that 
found in connection with pyelitis, and a differential 
diagnosis is only possible by a careful consideration 
of the cellular elements found in the sediment. In 
prostatitis there is an excess of cells from the 
prostatic urethra, together with an occasional cell 
from the neck of the bladder, and spermatozoa. 
The presence of casts from the straight tubules of 
the kidney is, on the other hand, indicative of 
pyelitis, and upon their presence the differential 
diagnosis is chiefly based. Rarely, casts of pros- 

12 



178 CLINICAL EXAMINATION 

tatic ducts are found. These are, however, irregu- 
lar in outline, much larger than renal casts, and in 
addition may have spermatozoa attached to them. 

Urethritis is, as the name implies, an inflam- 
mation of the urethra. It is rarely necessary to 
examine the urine to establish a diagnosis of this 
disease. Most commonly urethritis is due to a 
local infection of the urethral mucous membrane 
by the gonococcus, but it may also proceed from 
irritation caused by the long continued elimina- 
tion of irritants, e. g. cantharides and turpentine. 
Finally, it may occur in connection with infec- 
tious diseases. The urine, when voided, is at first 
cloudy, but as the products of inflammation are 
washed out of the urethra it becomes clear. In 
severe cases the urine may be bloody, as well as 
cloudy, and in the sediment are pus (in abundance 
when due to gonorrhoea), blood, and shreds of 
urethral epithelium. 

Blood in the Urine. — When the urine contains 
much blood, a diagnosis from an examination of 
the urine is frequently a matter of great difficulty. 
Severe hemorrhages usually occur from the pelvis 
of the kidney and the neck of the bladder, in con- 
nection with the passage of calculi or the presence 
of morbid growths. If due to calculi, the corpora 
delicti are found in the sediment ; but, as has been 
previously stated, morbid growths are seldom passed 



OF THE URINE, 179 

with the urine save when so situated that bits of 
the neoplasm may be dislodged by the passage of a 
catheter, or caught in the eye of the instrument. 

Pus in the Urine — When present in excess, 
pus is indicative of inflammation. It is not, per 
$e, diagnostic of any one affection. To determine 
its source, it is necessary to consider the nature 
of the cellular elements with which it is associated. 
Even then, owing to the similarity of the various 
types of epithelium, it is not always easy to locate 
the inflammatory process. Especially is this the 
case among females, in whom a suppurative pro- 
cess in the urinary organs is always accompanied 
by an excess of vaginal epithelium, in addition to 
other cellular elements, e. g. epithelium from the 
bladder and renal pelvis. The especial features 
of distinction between bladder and vaginal epi- 
thelium have already been discussed (vide page 
103). In addition, it may be stated that generally 
the amount of epithelium present is greater than 
can be accounted for by the amount of pus. With 
a cystitis, there is always pus in the urine. When 
unaccompanied by pus, an excess of epithelium is 
probably vaginal. 

In pyelitis the characteristic clump formations 
consist of pus corpuscles mixed with small round 
cells only. Under such conditions, the excess of 
large polygonal plate cells may be ignored. 



180 CLINICAL EXAMINATION OF THE URINE. 

Thus, when the sediment contains an excess of 
blood or pus, together with a few other elements, 
the diagnosis, satisfactorily or unsatisfactorily, 
must be made by a process of inquiry similar to 
the above. 



APPENDIX A. 

METHOD OF RECORDING EXAMINATIONS. 

For ordinary use, sheets of paper are printed in the 
manner indicated below, and as each test is made the 
result is indicated b} T abbreviations, more or less 
rational, more or less arbitrary, which are affixed to 
the spaces left for the purpose. 





ANALYSIS OF 


URINE. 


Name 




Date 


Amount in 24 hours = 
Color = 
Odor = 
Reaction = 


Solids by sp. gr. = 
Sp. gr. = 
Sed. = 


Uph. = 
Ixl. = 


U= Cl = 
U= Sf = 


E. P. = 
A. P. = 


Alb. = 

Quantitative. 

Sediment. 


Sugar = 
<U = 
(Cl = 


Bile pigment = 
H 8 P0 4 = 
Sugar == 


Diagnosis. 






Remarks. 







182 CLINICAL EXAMINATION 

The abbreviations used upon the blank forms are : 
Uph. (urophaeine), Ixl. or Ind. (indoxyl), CI (chlorides). 
U (urea), U (uric acid), Sf. (sulphates), E. P. (earthy 
phosphates), A. P. (alkaline phosphates), sp. gr. (spe- 
cific gravity), Sed. (sediment), Alb. (albumen), etc. 

The same plan maj- be incorporated into book form 
at a proportionate cost, and for those who make nu- 
merous examinations and keep permanent records the 
book form prefaced by a lettered index is perhaps 
more serviceable and convenient than the separate 
sheets. 

The common abbreviations used in recording results 
are : + for increased ; — for diminished ; N. for nor- 
mal. For great increase or great decrease : gt. + and 
gt. — , respectively, may be used ; similarly si. + and 
si. — for slight increase and slight decrease. Other 
abbreviations, according to the habit and convenience 
of the recorder, may equally well be adopted. 

Differential Diagnosis. 

The diagnosis between the different diseases of the 
urinary apparatus is made chiefly by exclusion. 

It has already been shown that, even in a single 
affection, the characters of the urine vary with the 
severitj 7 ' and extent of the process ; furthermore, that 
urinary diseases exhibit a great tendency to combine 
with one another. Obviously, an absolute standard, to 
which an unknown specimen of urine should conform, 
is out of the question. In other words, a urinary dis- 
ease is not accompanied by a urine of specific charac- 
ters, but of characters which will vary ; exhibiting, now 
only evidences of a more or less intense form of a sin- 



OF THE URINE. 183 

gle disease, now evidences of a more diffuse process, in 
which the characters of the dominant affection are the 
more obvious. 

In order, then, to make a diagnosis, it is highly 
important in every case, first, to know the " typical " 
or possible characters which are commonly associated 
with each form of disease ; and secondly, having made 
an accurate examination of an unknown specimen of 
urine, to harmonize so far as is possible the discovered 
characters with those known to be associated with this 
or that disease. Finally, it becomes possible only 
b}' the application of the above principles to say of 
an unknown specimen, " It probably belongs to this 
disease because, on the whole, it cannot belong to 
that." 

To illustrate this method of making diagnoses, the 
following examples are offered, followed by a brief 
consideration of the diagnosis in each case. 

1. Amount in 24 hours = 1000 c.c. Sp. gr. 1024. 
Color = high. Sed. much. 
Reaction = acid. 

Uph. = + U = + CI = si. — E. P. si. + 

Ixl. = N. u = gt. + Sf = N. A. P. si. -f 

Alb. = 0. Sugar = 0. Bile pigment = 0. 

Sed. Amorphous urates. 

2, Amount in 24 hours = 800 c.c. Sp. gr. = 1010. 
Color = smoky. Sed. = considerable. 
Reaction = acid. 

Uph. = - U = - C1 = N. E. P. = - 

Ixl. = + U = N. Sf = N. A.P. = - 

Alb. = 1%. 

Sed. Few free blood globules. Renal epithelium. Epithe- 
lial, blood, fibrinous, granular, and brown granular 
casts. 



184 CLINICAL EXAMINATION 

3. Amount in 24 hours = 1020 c.c. Sp. gr. = 1030. 
Color = high. 

Reaction = acid. 

Uph. = N. ft = N. + CI = gt. + E. P. = N. 

IxL = N. U = N. + Sf=gt. + A.P. = sl. - 

Alb. = si. trace. 

Sed. Many uric acid crystals. Considerable blood and renal 

epithelium. Numerous hyaline casts, many of which 

have renal cells and blood adherent. 

4. Amount in 24 hours = 470 c.c. Sp. gr. = 1030. 
Color = high. Sed. = considerable 
Reaction = acid 

Uph. = + ft = gt. + CI = - E. P. = N. 

Ixl. = gt. + U = gt, + Sf = N. A. P. = - 
Alb. = 2%. 

Quant. jU = 17-6. H 8 P0 4 = 0.664. 

^ I CI = 0.598. Sugar = 0. 

Sed. Numerous hyaline, granular, and fatty casts. Fatty 
renal epithelium. 

5. Amount in 24 hours = 1500 c.c. Sp. gr. = 1008. 
Color = pale. Sed. = considerable. 
Reaction = acid. 

Uph. = - ft = - CI = - E. P. = - 

Ixl. =- U = - Sf = - A.P. = - 

Alb. = large trace. 
QuantJU = 18. 

( CI = 2.72. 
Sed. Hyaline and granular casts. 



Amount in 24 hours — 1230 c.c. 
Color = si. pale. 
Reaction = acid. 


Sp gr. r^ 1012. 
Sed. = slight. 


Uph. = - ft - - CI = N. 
Ixl. = N. U = sl.+ Sf=N. 


E. P. = - 
A. P. = - 


Alb. = very si. trace. 
Quant. |U= 15.74. H 3 P0 4 = 
f CI- 4.18. 


0.96. 


Sed. An occasional pure hyaline cast. 



OF THE URINE. 



185 



Amount in 24 hours = 3450 c.c. Sp. gr. = 1012. 

Color = pale. Sed = slight. 

Reaction = acid. 

Uph = much - t = - CI = - E. P. = - 

Ixl. = N. U = - Sf=N. A.P. = sL- 

Alb. = \%. 

Quant. jU = 35.9. H 3 P0 4 = 2 24. 

^ ( CI = 10.4. 

Sed. Hyaline, granular, and waxy casts. 



Amount in 24 hours = 2400 c.c. 

Color = pale. 

Reaction = acid. 

Uph. = - U = - CI = - 

Ixl. = N. U = N. Sf=sl.+ 

Alb — - 7 - / 

A1U - — lO/o* 

Sed. Normal blood and pus, excess of vaginal epithelium. 
Hyaline and granular casts. 



Sp. gr. = 1010. 
Sed. = considerable. 

E. P. = - 
A. P. = + 



Amount in 24 hours = 500 c.c. 
Color = high. 
Reaction = acid. 

Uph. = N. U = + CI = N. 
Ixl. = si. + U = + Sf = N. 

Alb. = very si. trace. 
TJ = 17-5. 



Sp. gr. = 1024. 
Sed. = considerable. 

E. P. = N. 
A. P. = N. 



Quant. 



Cl= 4( 



Sed. Hyaline casts. 



10. 



Color = N. 
Reaction = acid. " 
Uph. = N. U = N. 

Ixl. = N. U = N. 

Alb. = large trace. 
Quant. |U = 25. 
^ I CI = 4.60. 



Excess of mucus. 




1200 c.c. 


Sp. gr. = 1019. 




Sed. = considerable. 


C1 = N. 


E. P. - N. 


Sf = N. 


A. P. = - 


H 3 P0 4 = 2.15. 





186 CLINICAL EXAMINATION 

Sed. Renal epithelium, some of which is fatty. Hyaline and 
granular casts, some having oil globules adherent 
An occasional epithelial and fatty cast. Occasional 
blood globule, both free and adherent to some casts. 

11. Amount in 24 hours = 1150 c.c Sp. gr. == 1012. 
Color — smoky. Sed. = considerable. 
Reaction = acid. 

Uph. = N. U = - CI = - E. P = N. 

Ixl. = + U = + Sf=N. A.P. = N. 

Alb. = li to 2%. 

Sed. Epithelial, fibrinous, hyaline, fine granular, and fatty 
casts. Renal cells, some of which are fatty. Numer- 
ous blood globules, some pus. 

12. Amount in 21 hours = 1350 c.c. Sp. gr. = 1015. 
Color = pale. 

Reaction == acid. 

Uph. = - U = - CI = N. E. P. = - 

Ixl. = si. - U = + Sf=N. A. P. = N. 

Alb. = 1%. 

Quant. | U- 22.6. H 3 P0 4 = 1 2 

^ Id = 6. 

Sed. Numerous hyaline, coarse, and fine granular casts. 
Fatty and epithelial casts. Considerable fatty renal 
epithelium. Little pus, blood, and bladder epithelium. 

13. Amount in 24 hours = 1850 c.c. Sp. gr. = 1012. 
Color = pale. Sed. = considerable. 
Reaction = acid. 

Uph. = - t - - CI = si. - E. R = - 
Ixl. = +. U = N. Sf=N. A.E. = - 

Alb. = 1%. 

HoP0 4 = 1.51. 



QuantJ U = 23 ' 4 ' 
I CI = 4.34. 



Sed. Numerous hyaline, fatty, and granular casts. Fatty 
renal epithelium. Compound granule cells. Pus 
corpuscles free and in clumps. Normal blood glob- 
ules and small round cells. 



OF THE URINE. 187 

14. Amount in 24 hours - GOO c.c. Sp. gr. == 1012. 

Color = si. smoky. Sed. = considerable. 

Reaction = acid. 

uph. = - u = - a = - E. P. = - 

Ixl. = N. U= Sf = A. P. = - 

Alb. = i to 1%. 

Sed. Numerous large granular, coarse granular, fatty, and 

waxy casts. Granular and fatty renal epithelium. 

Compound granule cells. Cholesterine crystals. 

Blood. 

f5. Amount in 24 hours = 1770 c.c. Sp. gr. = 1014. 

Color = si. pale. Sed. = considerable. 

Reaction = acid. 

Uph. = N. U = - CI = si. - E. P. = - 

Ixl = si. - U = N Sf = N. A. P. = - 

Alb. = A%. 

Sed. Much blood; little free renal epithelium; hyaline and 

granular casts ; few blood and epithelial casts ; very 

few fatty casts. 

16. Amount in 24 hours = 1760 c.c. Sp. gr. 1015. 
Color = pale. Sed. = considerable. 
Reaction = acid. 

Uph. =- U = - CI = N E. P. = N. 

IxL = + U = + Sf=-N. A. P. = N. 

Alb. = itoi%. 

Sed. Hyaline, coarse, fine granular, and fatty casts. Renal 
epithelium, much of which is fatty. 

17. Amount in 24 hours = 1800 to 2400 c.c. Sp. gr. = 101SJ. 
Color = si. pale. Sed. = considerable. 
Reaction = acid. 

Alb. = 1%. 

Sed Numerous hyaline casts, all with more or less fat drops 

adherent. No fatty casts ; an occasional granular 

cast. Renal epithelium, most of which is fatty. 

Small quantity of pus, and numerous compound 

granule cells. 



188 CLINICAL EXAMINATION 

18. Amount in 24 hours = 1360 c.c. Sp. gr. = 1022. 

Color = high. Sed. = considerable. 

Reaction = acid. 

Uph. = N. U = + CI = N. E. P. = N. 

Ixl. = N. U = + Sf = N. A. P. = N. 

Alb = si. trace. 

Quant. | U- 35.02. H 8 P0 4 = 3.250. 

^ I CI = 19.30. 

Sed. Chiefly uric acid crystals. Numerous hyaline and 
granular casts, many of which are of large diameter 
and have blood globules and renal cells adherent. 
Little free blood and renal epithelium. 



Amount in 24 hours = 
Color = pale. 
Reaction = acid. 
Uph. = - U = - 


2350 c.c. 
Cl = - 


Sp. gr. = 1012. 
Sed. = slight, 

E. P. = - 


Ixl. = - U = - 


Sf =- 


A. P. = -- 


Alb. = £%. 

n , ( U = 28 8. 

Quan Mci= 3.24. 







Sed. Chiefly hyaline and fine granular casts. An occasional 
blood, epithelial, and fatty cast. Little free blood. 
Fatty and granular renal epithelium. 



Amount in 24 hours = 1920 c.c Sp. gr. = 1013J. 

Color = N. Sed. = considerable. 

Reaction = acid. 

Uph. = N U = N. CI = - E. P. = - 

Ixl. = N. U = si. + Sf = N. A. P. = N. 

Alb. = si. trace. 

= 41.5. H 3 P0 4 = 4.20. 

! Cl = 7.52. 

Sed. Large amount of uric acid. Numerous hyaline and fine 
granular casts. An occasional epithelial and fibrin- 
ous cast. Little free blood and renal epithelium. 



Quant. {U; 



OF THE URINE. 189 

21. Amount in 24 hours = 1150 c.c. Sp. gr. = 1013. 

Color = N. or si. pale. Sed. = considerable. 

Reaction = acid. 

Uph. = - = N. Cl=sl. - E.P. = - 

Ixl. = - U= Sf= A.P. =N. 

Alb. = si. trace. 

Sed. Much pus, free and in clumps. Bladder epithelium, 
free and in shreds. Very little free abnormal blood. 
Little renal epithelium, some of which is slightly 
fatty. Occasional medium and large round cell. 
Occasional caudate cell. Fine granular, brown gran- 
ular, blood, and fibrinous casts. Occasional pure hy- 
aline casts (of small and medium diameter), some 
with blood, pus, and fat drops adherent. 



22. 



Amount in 24 hours = 


1275 


• c.c. 


Sp. gr = 1020. 


Color = N. 






Sed. = considerable, 


Reaction = acid. 








Uph = N. fi = N. 




C1 = N. 


E. P. = N. 


Ixl. = N. U = + 




Sf = N. 


A. P. = - 


Alb. = large trace. 








*-JS:"JS 




H 3 P0 4 = 


1 976. 



Sed. Eew abnormal blood globules. Excess of renal cells, 
some of which are fatty. Considerable number of 
hyaline and granular casts, some of which have a 
few blood and oil globules and renal cells adherent. 



The Inferences. 

1. A simple concentrated urine of febrile character. 
The increase of uric acid suggests insufficient oxidation, 
and in combination with the diminution of the chlorides 
might fairly illustrate a urine of pneumonia. 

2. The character of the sediment limits the process 
to the kidney and the amount of urine to the parenclrym- 



190 CLINICAL EXAMINATION 

atous affections. The characteristic fatty elements of 
the chronic parenchymatous nephritis are absent, whereas 
everything about the urine is typical of acute nephritis 
in its early stage. 

3. A case of active lrypersemia due to the irritating 
action of uric acid crystals. 

4. The amount of urine and the character of the sedi- 
ment limit the diagnosis to a parenchymatous affection, 
either the chronic form or the acute in the fatt} T stage. 
Were it the latter, one would expect less albumen and 
more urine ; hence the probability is that it is a case of 
chronic parenclrymatous in the active stage. 

5. The great diminution of the solids, the small 
amount of albumen, and the character of the sediment 
suggest unquestionably chronic interstitial nephritis. 

6. Here again the case seems to be one of chronic 
interstitial nephritis, although in both this and the pre- 
vious case the possibility of advanced amyloid degen- 
eration cannot be definitely excluded. 

7. The quantity of the urine alone limits the possi- 
bility to four conditions, viz. recovery from acute ne- 
phritis, interstitial, amyloid degeneration, and diffuse 
nephritis. Waxy casts are not as a rule associated 
with acute disease, and acute nephritis is very improb- 
able. Were it not for the known quantitative amount of 
so] ids, amyloid degeneration and interstitial nephritis 
could not be differentiated ; but the almost normal quan- 
tity of solids excludes interstitial, and therefore diffuse 
nephritis, and suggests unquestionably amyloid degener- 
ation, for in this disease the eliminating function is not 
for a long time materially embarrassed. 



OF THE URINE. 191 

8. In this case the diagnosis lies between interstitial 
nephritis and amyloid degeneration ; without a quan- 
titative estimation of the solids, a positive diagnosis 
cannot be made. The absolute increase of indoxyl is 
more suggestive of interstitial, than the greater per cent 
of albumen is of amyloid degeneration. The excess of 
vaginal epithelium may have a causal relation to the 
blood and pus, and in all probability is due to a con- 
comitant menstrual flow, or some irritation about the 
cervix uteri. 

9. In this case the sediment is not indicative of an 
irritation nor inflammation, hence neither a nephritis 
nor yet an active hypersemia. The onl}' possibility is 
therefore a passive hypersemia, the characters of which 
it best fulfils. 

10. The general characters of the urine suggest 
active hypersemia, acute nephritis in the fatty stage, 
and chronic parenchymatous nephritis. As against the 
last affection there is the presence of renal cells and 
blood, the lack of positive and characteristic fatt} T ele- 
ments, the relatively small amount of albumen, and a 
rather large quantity of urine. It is quite safe to ex- 
clude the chronic parenchimatous disease. If it were 
a case of active hypersemia, one would expect naturally 
a higher specific gravity, and, unless a very severe case, 
the absence of fatty elements ; and finall} T , the presence 
of some bit of concretion or crystalline form to which 
the irritation might be ascribed. In the second stage 
of acute nephritis the urine is characterized by an in- 
crease in amount, together with an increase of the spe- 
cific gravity, diminution of albumen, and the appearance 
of fatt} T elements in the sediment. These characters 



192 CLINICAL EXAMINATION 

are present in this case, and although in severe cases 
brown granular and fibrinous casts may be present, 
their absence does not preclude the diagnosis of acute 
nephritis passing through the fatty stage. 

11. A more tj-pical example of the former. 

12. Another case of acute nephritis in the second 

stage. 

13. The amount of urine excludes everything but 
recover} 7 from acute or interstitial nephritis, amyloid 
degeneration, and diffuse nephritis. The abundance 
of fatty elements in the sediment and the compound 
granule cells are ver} 7 suggestive of chronic parenchym- 
atous, yet the quantity of urine and the per cent of 
albumen are not in conformity with this view. The in- 
creased amount of urine, the diminution of the solids, 
and the relatively small quantity of albumen favor in- 
terstitial. Hence, if both these coexist, the conditions 
will be satisfied, and the diagnosis of diffuse nephritis 
will be the result. The pus and small round cells are 
equally indicative of a complication with pyelitis or 
prostatitis, but the disease of the kidney makes it more 
probable that it is the pelvis that has become involved. 

14. The excess of fatty elements in the sediment 
makes a diagnosis of chronic parenchymatous almost 
certain ; yet the smoky color of the urine and the 
presence of blood in the sediment bespeak an acute 
process or exacerbation, which in all probability has 
occurred. The elimination of cholesterine crystals may 
have caused irritation of the renal tissue. 

15. As in cases 7 and 13, the diagnosis lies between 
interstitial nephritis, amyloid degeneration, diffuse, and 



OF THE URINE. 193 

recovery from acute nephritis. Without a quantitative 
estimation of the solids, no positive diagnosis between 
these possibilities can be made. If it were a case of 
recoveiy from acute nephritis, it would be natural to 
expect a higher specific gravity, and not a considerable 
amount of blood. On the other hand, it is not usual 
for fatty casts to exist in the sediment of interstitial 
nephritis or anryloid degeneration. If it were a diffuse 
nephritis, a greater quantity of fatty elements would in 
all probability be present. Some combination, there- 
fore, may be assumed to exist. The quantity of urine, 
the low specific gravity, and the per cent of albumen, 
are equally in favor of interstitial nephritis and amy- 
loid degeneration, whereas the blood, renal epithelium, 
and fatty casts are suggestive of an acute nephritis in 
a stage of beginning convalescence ; and on the whole 
the conditions are best satisfied by assuming that an 
acute nephritis is superimposed upon an interstitial 
nephritis or amyloid degeneration. 

16. The same considerations hold in this case as 
in the last, but here the fatty elements predominate, 
whereas the traces of acute disease are wanting. Aside 
from the quantity of urine, its characters are not in- 
compatible with chronic parenchimatous nephritis ; but 
the quantit}' cannot be excluded from the consideration, 
and in all probability a combination of interstitial (or 
amyloid degeneration) and chronic parenchymatous 
nephritis exists. It may be considered, therefore, to 
be a case of diffuse nephritis. 

17. As in the two preceding cases, the same exclu- 
sions may be made. Like the last, fatt}' elements pre- 
dominate, which make the consideration of chronic 

13 



191 CLINICAL EXAMINATION 

parenchymatous nephritis imperative. There is, too, 
a relatively high per cent of albumen, which, without 
the signs of a recent active inflammation, make an 
acute nephritis improbable. The quantity of albumen 
is rather high for interstitial nephritis, although not 
for amyloid degeneration or chronic parenchymatous 
nephritis. The combination of the latter disease with 
interstitial nephritis or amyloid degeneration may be 
said to exist, but without a quantitative estimation of 
the solids, it cannot be positively affirmed with which 
the parenclrymatous process is combined. 

18. The uric acid cr} T stals furnish the key of the 
situation. Aside from the albumen and sediment, the 
urine, as the quantitative estimation of the solids 
shows, is not abnormal. The sediment, however, is 
indicative of a slight irritation, which may be readily 
accounted for by the action of the uric acid crystals. 
Therefore an active hyperemia due to the irritation 
caused lry these crystals is quite sufficient as a 
diagnosis. 

19. Here, again, the same exclusions as in cases 7, 
13, 15, 16, and 17 may be made. It is unnecessary 
to 2:0 over again the same considerations as were made 
in those cases. The diminution of the normal constitu- 
ents is in a great measure relative, although some ab- 
solute diminution also exists. The blood and epithelial 
casts indicate the existence of an acute process, and 
the fatt} T elements that the acute process has in a meas- 
ure subsided, i. e. that it has progressed to the second 
or fatty stage. In fact, the features of acute nephritis 
in its fattj T stage are typicall} T illustrated. It cannot 
be positively affirmed, however, whether an interstitial 
or amyloid process coexists. 



OF THE URINE. 195 

20. The absolute amount of solids excludes inter- 
stitial nephritis, amyloid degeneration, and, together 
with the absence of fatty elements, diffuse nephritis. 
Recovery from acute nephritis seems to be pretty well 
established. The excess of uric acid may be due to 
some defect of the oxidative processes or other cause 
of increased elimination of uric acid, but in all proba- 
bility has no immediate relation to the pathological 
processes. 

21. The character of the sediment alone is indicative 
of some active inflammatory process not confined to 
the kiclne}-. The pus, caudate, and small round cells 
signify a destructive process connected w T ith the renal 
pelvis and the casts, — that the renal tissue itself has 
been involved. The bladder epithelium and large round 
cells show, too, that the bladder and its neck have not 
escaped in the diffuse process. It cannot be affirmed 
which of the affections is primary. The indications at 
present are that a pyelo-nephritis exists which may 
have originated in cystitis. The per cent of albumen 
is not sufficiently large to indicate any considerable 
involvement of the renal tissue, and furthermore it is 
not greater than might readily be accounted for by the 
pus and blood. 

22. The process is evidently acute, but it has lasted 
long enough for fatty changes to occur. Fatty ele- 
ments alone are associated with severe cases of active 
hyperemia, and acute and chronic parenchymatous ne- 
phritis. They are not, however, sufficiently numerous, 
nor is there so high a per cent of albumen, as to sug- 
gest the chronic nephritis. Between a severe form of 
active hyperemia and an acute nephritis no positive 



196 CLINICAL EXAMINATION 

diagnosis in many instances can be made. Such seems 
to be the case here. On the one hand, during the fatty 
stage of acute nephritis one might expect a larger 
quantity of urine, as well as a larger per cent of 
albumen, than are present in this case. On the other 
hand, it is rare, although not impossible, for fatty 
changes to occur in active hyperemia without evi- 
dences of a more intense irritative process. While 
it is impossible to say to which this case is to be 
referred, yet on the whole the present indications 
are more in favor of active hyperemia than of acute 
nephritis. 



OF THE URINE. 197 



APPENDIX B. 

TABULAR ARRANGEMENT OF THE CHARACTERS OF THE 
URINE IN THE MORE IMPORTANT URINARY DISEASES. 

For the purposes of easy reference, those features of 
the urine upon which the diagnosis is based have been 
arranged in tabular form, and incorporated into the 
following pages. While, as has so often been remarked, 
it is impossible to make any hard and fast distinctions 
as to what may properly constitute this or that disease, 
yet it is often convenient to see at a glance a group of 
tolerably constant symptoms, to which those obtained 
from a clinical examination may be quickly compared. 
In all cases, after a thorough comprehension of the 
nature of the different forms of disease, a thoroughly 
consistent deduction concerning the features discovered 
in an unknown specimen is far superior to any 
mechanical adaptation of symptoms to a table. 



198 



CLINICAL EXAMINATION 



S3 

s 

K 

a: 


Free blood and renal cells, frequently 
colored more or less brown. 

Casts. Hyaline and fine granular, with 
blood globules and renal cells adhe- 
rent. Occasional blood and epithe- 
lial casts. Brown granular and fibri- 
nous casts in addition to the above. 


Virtual absence of blood, no excess of 

renal cells. 
Casts. Hyaline and fine granular (of 

small diameter). Rarely a blood and 

epithelial cast. 


Brown -colored. Free abnormal blood 
and an excess of renal cells colored ^ 
brown. 

Casts. Blood, epithelial, brown granu- 
lar, and fibrinous. Occasional hya- 
line and fine granular. 

Fatty elements, cells, atid casts. The 
hyaline and fine granular casts per- 
sist while brown granular and fibri- 
nous disappear. 

Hyaline and fine granular casts, an oc- 
casional blood cast, a few blood glob- 
ules and renal cells. A few remain- 
ing fatty elements 


Considerable amorphous urates. 

Fatty renal epithelium and compound 
granule cells. 

Casts. Fatty (of large diameter often), 
hyaline and finegranular. Near the 
fatal termination, waxy casts. 


C3 

< 


si. trace 

in severe 
cases, 


© 
© 


X T i 

1 --W _£* 


up 

-to 


c 


-f- or — 

(chlorides may or 
may not be di- 
minished) 


about normal 

absolute — 

+ relative -f- 

(U and U may be 

absolutely -f) 

chlorides follow 

the effusions 


absolutely — 
relatively + 

increase 

(chlorides re- 
appear) 

relatively — 
absolutely about 

N. 


relatively -f- 

(except CI and P) 

absolutely — 

(except U) 


qq 


o 

o 


rid 

a # fcc 
2 


high or low, ac- 
cording to oc- 
clusion of tu- 
bules, amount 
of blood and 
albumen, 
less than N. 

low 


00 

CO 
(M 

o 

r^ 
JOB 


C3 

c 

o 


© 

p< 
u 

o 


high or pale 


dark brown 
(smoky) 
or black 

light smoky 

N. or pale 




< 

0? 


+ 1 

>> 

1 3 


(600-1000 c.c. ) 


(300-500 c.c.) 

increase 

(800-1000 c.c.) 

(2500-3000 c.c.) 


(500-800 c.c.) 


< 

n 


c3 

a 

© 

Pi 

>> 

i 
© 
< 


c3 

a 
>> 

| 


Acute Par. Nephritis 
1st stage . . . 

2d stage . . . 
3d stage . . . 


J3 * 

If 

£ ® 

§3 

3 



OF THE URINE. 



199 



*4 
© 
■ 
00 

3 
o 

X! 
0> 

c 

ep* 

be 
a 

S 
► 

o 

c8 

.5 

00 SR 

08 » 

° 2 


An occasional renal cell. 

Casts. Hyaline and fine granular (small , 

medium, and in advanced cases, 

large diameter). 
Same with waxy casts previous to the 

fatal termination. 


.2 

GO 

U 
CD 
4a 

P 

-: 

o> 

S 

c8 

m 


Considerable pus and blood. Caudate 
cells from superficial layers of pelvis 
during early stages. 

Bits of concretions (if due to these). 

Characteristic arrangement of pus, 
blood, and cells together in clumps. 

If tubules of kidney are involved, hy- 
aline, epithelial, and granular casts. 

Similar to the acute stage. Not so 
abundant, and in place of caudate 
cells are small round cells from deep- 
er layers. 


Pus and blood, excess of bladder epi- 
thelium (varies with cause and com- 
plication ). 

Very turbid. Bacteria. Crystals of 
ammonium urate, triple phosphate, 
disintegrated pus corpuscles. Blood 
and bladder epithelium. 

Pus, blood, and bladder epithelium. 


-H 

5? 


e normal. 


si trace pro- 
gresses to 

k~h% usu- 
ally 


trace 
varies with 
the pus and 
blood 

ditto 


same as in 
Pyelitis 

ditto 
ditto 


1 

CD 

i 

"a 


slowly from th 

rel. and abs. — 

except indoxyl 

which is rel. N. 

.". abs. -f- 

ditto 


more nearly nor- 
mal 
+ 
U diminished. 


1 

u 
o 

to 


+ 1 

r* CO 
O) £1 


o 


ne varies but 
low (1010 ±) 

low (1005 ±) 


low, but on the 
average higher 
than in inter- 
stitial 


+ 1 


_1_ £ £ 

"TO £ 


o 

p. 


ages the uii 
pale 

pale 


© 

ft 


high 
pale 


high 

pale 
pale 


g © 
o 

CO 


In the early st 
(2000-4000 c.c ) 

decrease 

N. or — 


+ 

(2500-4000 c.c.) 

decreases before 

death 


1 1 


at first acid 
then alkaline 

ammoniacal 
"ropy " 

usually acid, 
not ropy 


ft a) 
* be 

. CO 

Si 

O GO 

'P * 

£* 


Chronic Interstitial 
Nephritis 
2d stage ... 

3d stage . . . 


.2 
1 

0> 
bO 

0> 

p 

< 


Pyelitis, Acute . . 
(general febrile char- 
acters) 

Pyelitis, Chronic . . 


Cystitis, Acute . . 

Cystitis, Chronic . . 
(untreated) . . . 

(treated) .... 



200 CLINICAL EXAMINATION 



APPENDIX C. 

TABULAR ARRANGEMENT OF HELLER'S CHEMICAL 

TESTS. 

Physical Properties. 

Color. — Pale, normal, high, or dark. 

Odor. — 

Reaction. — Acid, neutral, or alkaline. 

Sp. gr. — By urinometer. 

Sediment. — Slight, considerable, or much. 

Normal Constituents. 

Urophceine (Uph.). — H 2 S0 4 + double quantity of Ur. = imme- 
diate brown color. 

Indoxtjl (Ixl.). — HC1 + 3 gtt. HN0 3 -f 30 gtt. Ur. = amethyst 
color. 

Urea (U). — 1 gtt. Ur. -f 1 gtt. HN0 3 in wgl. = nit. urea cryst. 
in 20 to 30 minutes. 

Uric Acid (U). — ± tt. Ur. + HCI = U cryst. in 24 hours. 

Chlorine (CI). — Ur. -f HN0 3 + AgN0 8 (l:8) = solid ball of 
Ag CI, if normal. 

Sidphates (Sf ) — \ tt. Ur. + BaCl 2 sol. (sat. sol. + \ HCI) = Ppt. 
(J concav. of tt.). 

Earthy Phosphates (E. P.)- — I tt. Ur. + NH 4 OH = Ppt. \ to \ 
in. in tt., if normal. 

Alkaline Phosphates (A. P.). —Filtrate from E. P. + MgS0 4 sol. 
(sat. sol. MgS0 4 4- NH 4 C1) = Ppt. \ to f in. in tt., if normal. 

Abnormal Constituents. 

Albumen (Alb.) — Heat or HN0 3 = Coagulum or zone. 

Bile Pigments. — Ur. spread on plate -f- 1 gtt. HN0 3 = prismatic 
rings. 

Sugar. — Ur. in tt. + NaOH + CuS0 4 + heat = Ppt. yellow 
(Cu 2 0). 

Sediment. — Let settle and Examine by microscope. 



OF THE URINE. 201 

Experience will show that, in performing these tests, 
it is more convenient to examine for albumen imme- 
diately after urophseine and indoxyl ; for if present in 
any considerable amount, albumen must be removed in 
order that its presence shall not interfere with the 
proper reaction of the subsequent tests. 

The nitric acid test for albumen abridges several 
other tests, viz. : — 

A zone above the junction of the urine and acid, 
in the urine, indicates an excess of urates and uric 
acid. A zone below the junction, in the acid, indi- 
cates the presence of nitrate of urea, hence an excess 
of urea. 

If bile pigment is present, the characteristic play of 
colors will be observed. 

The presence of iodine is indicated by a fine brown 
granular zone where the albumen zone is usually found, 
i. e. between the urine and acid. 

Finally, if the amount of albumen present is small, 
the chlorides may be tested for in the same glass, after 
the above determinations have been made, by first stir- 
ring the urine and acid together with a glass rod, and 
then adding a drop of AgN0 3 . 



INDEX. 



Abnormal blood disk, 113. 
Abnormal coloring matters, 64. 
Absce>s of kidney, 171. 
Absolute amount, 5. 
Accidental constituents, 72. 
Acid fermentation, 82. 
Active hyperemia, 151. 
Acute parenchymatous nephritis, 

155. 
Acute yellow atrophy, 139. 
Addison's disease, 141. 
Albumen, 47. 

acid and alkali albumens, 48. 
Albuminuria, 47. 

true, 53. 

false, 54. 

causes, 54. 
Albuminuria of adolescence. 54. 
Alkalies, 76. 

Alkaline fermentation. 84 
Alkapton, 57. 
Ammonia, 75- 
Amount, 9. 

Amyloid degeneration, 167. 
Anaemia and chlorosis, 141. 
Analysis of calculi, 131. 
Anuria, 12, 134. 
Arsenic in the urine, 79. 
Arseniuretted hydrogen poisoning, 
139. 



Bacillus tuberculosis, 

Bacteria, 123. 

Biliary constituents, 64. 



124 



Bilirubin, 103. 

Bladder epithelium, 108. 

Blood disks, 112. 

normal, 113. 

abnormal, 113. 
Blood in the urine, 66, 178. 
Bowman's theory, 3. 

Calcic carbonate, 97. 
Calcic oxalate, 84, 92. 
Calculi, 128 

primary, 129. 

secondary, 129. 

nucleus, body and crust, 130. 

compound, 130. 

number of, 130. 

to examine, 131. 
Cancer cells. 125. 
Casts, 114. 

theories of origin, 114. 

tabular classification, 116. 

hints on examination for, 120. 
Changes of urine on standing, 20. 
Characters of urine in 

active hyperemia, 151. 

passive hyperemia, 153. 

acute nephritis, 155. 

chronic parenchymatous ne- 
phritis, 161. 

chronic interstitial nephritis, 
165. 

amyloid degeneration, 167 
Chemical characters of urine, 22. 
Chlorides, 39. 



204 



INDEX. 



Chlorosis and anaemia, 141. 
Cholera, 139. 
Cholesterine, 74, 100. 
Chronic cardiac diseases, 142. 
" diseases of spine, 141. 
' ; " bone, 141. 

liver, 140. 
" gout, 140. 

" interstitial nephritis, 163. 
" parenchymatous nephritis, 

160. 
" rheumatism, 140. 
Chyle and chyluria, 73. 
Classification of color, 16. 

" u sediment, 86, 87. 

Color, 16. 

Coloring matters of blood, 66. 
Combination of organic renal dis- 
eases, 169. 
Compound granule cells, 111. 
Concretions, 127. 
Consistency of urine, 7. 
Cystine, 98. 
Cystitis, 174. 
acute, 175. 
chronic, 176. 

Diabetes, 13. 
Diazo reaction, 138. 
Differential diagnosis, 182. 
Diseases of the skin, 142. 
Diseases of urinary membranes be- 
low the kidneys, 171. 
Diurnal variation, 9 
Donne's test for pus, 107. 
Drink and food, 9. 
Dropsy, 142. 

Earthy phosphates, 95. 
Echinococcus, 125. 
Entozoa. 125. 
Epithelium, 108. 

Etiology and pathology of nephri- 
tis, 145. 
Exercise, 9. 
Extraneous matter, 126. 



Fat, 72, 121. 
Fatty acids, 74. 
Fehling's test for sugar, 59. 
Fermentation of urine, 82. 

acid, 82. 

alkaline, 84. 
Fermentation test, 60. 
Fever urine, 136. 
Fibrin, 113. 

Filaria sanguinis hominis, 125. 
Foam on urine, 8. 
Forms of albumen, 48. 
Fungi, 122. 

General diseases, 133. 
Globulins, 48. 
Glycosuria, 56. 
causes, 62. 
Gmelin's test, 65. 
Gravel, 127. 

HEMATURIA, 67. 

Hemoglobinuria, 68. 

Heart diseases, 142. 

Heat test, 49. 

Heller's table of clinical tests, 200. 

Heller's test for sugar, 57. 

Hints on the examination for casts, 

120. 
Hippuric acid, 33, 92. 
Hydrobilirubin, 35. 
Hydronephrosis, 173. 
Hydruria, 13. 

Illustrative cases for diagnosis, 

183. 
Indican, 37. 
Indoxyl, 37. 
Inosit, 58. 

Intermittent fever, 137. 
Intestinal diseases, 139. 
Introduction, 1. 
Iodide of potassium, 76» 

Kreatine, 29. 
(Creatinine, 30. 



INDEX. 



205 



Lead in the urine, 77. 
Leucine and tyrosine, 63, 100. 
Leucocytes and pus, 105. 
Leucocythsemia, 141. 
Local diseases, 144. 
Ludwig's theory, 3. 

Malignant disease of 

abdominal viscera, 142. 
kidneys, 171. 

Manufacture of urea. 24. 

Measurement of blood disks, 72. 

Melanotic cancer, 142. 

Meningitis, 138. 

Mercury in the urine, 79. 

Metallic s:ilts, 76 

Method of recording examinations, 
181. 

Micrococcus Ureae, 19. 

Moore's test, 57. 

Morbid growths, 125. 

Mucus, 103. 

Mulberry calculus, 130. 

Murexide test, 30. 31. 

Musculus ferment, 19. 

Nature of the urinary excretion, 3. 
Neck of the bladder cells, 111. 
Nitric acid test, 50. 
Non-fatty acids, 75. 
Non-obstructive anuria, 135. 
Normal blood disk, 113. 

Obstructive anuria, 134. 
Odor, 17. 
Oliguria, 12, 134. 
Organic constituents, 23. 
Organized sediment, 103. 

Passive hyperemia, 153. 
Pelvic epithelium, 110. 
Pencilium glaucum, 122. 
Peptonuria, 48. 
Peritonitis, 137. 
Phenol, 34. 
Phosphates, 43. 
earthy, 43. 



Phosphates, alkaline, 44. 

Phosphaturia, 46. 

Phosphoric acid, 18. 

Phosphorus poisoning, 139. 

Phthisis, 141. 

Physical characters of urine, 7 

Polyuria, 11, 133. 

Pregnancy, 154. 

Preservation of sediments, 126. 

Prostatic cells, 111. 

Prostatitis, 177. 

Purpura hemorrhagica, 141. 

Pus in the urine, 105, 179. ■ 

Donne's test, 107. 
Pyelitis, 171. 

acute. 172. 

chronic, 173. 
Pyonephrosis, 173. 

Quantitative tests : — 
albumen, 50. 
chlorides, 40. 
phosphoric acid, 43. 
sugar, 59. 
urea, 25. 

Reaction, 18. 
Relative amount, 5. 
Renal casts, 114. 
Renal cells, 110. 
Rheumatic fever, 137. 

Saccharomyces, 122. 
Sand, 127. 
Sarcina, 123. 
Sarkine, 30. 
Scurvy, 141. 
Sediment, 81. 
Senile atrophy, 170. 
Small-pox, 139. 
Solids in the urine, 15. 
Specific gravity, 12. 
Spermatozoa, 121. 
Sugar, 56. 
Sulphates, 46. 
Suppression of urine, 134. 



206 



INDEX, 



Tables : — 

blood globules, 72. 

casts, 116. 

constituents of calculi, 129. 

characters of urine in more im- 
portant diseases, 198. 

Heller's clinical tests, 200. 

sediments, 87. 

urea, 28 

urinary constituents, 22. 
Tests : — 

bismuth, 61. 

Fehling's, 59. 

fermentation, 60. 

heat. 49, 70. 

Heller's, Moore's, 57. 

iron, 70. 

nitric acid, 50. 

sodium tungstate, 70. 

Teichman's, 69. 

Trommer's, 58. 
Tests for 

albumen, 49. 

alkaline phosphates, 44. 

blood, 69. 

chlorides, 40. 

earthy phosphates, 43. 

indoxyl, 38. 

sugar, 58. 

sulphates, 46. 

urea, 24. 

uric acid, 32. 

urophaeine, 36. 
To preserve urinary sediments, 126. 
Torula cerevisise, 123. 
Transparency of urine, 7. 



Trommer's test, 58. 
Typhoid fever, 138. 
Typhus fever, 139. 
Tyrosine, 63, 100. 

Urate of ammonium, 90. 
Urates, K, Na, and "mixed,' 
Urea, 23. 

Ureter epithelium, 109. 
Ureteritis, 173. 
Urethral cells, 111. 
Urethritis, 178. 
Uric acid, 30, 87. 

recognition of, 88. 
Urinary concretions, 127. 
Urinometer, 14. 
Urobilin, 35. 
Urohaamatin, 35. 
Urophaeine, 35. 
Uroxanthine, 36. 

Vaginal epithelium, 108 . 
Variations in 

amount of urea, 29. 

chlorides, 42. 

color, 16. 

hippuric acid, 33. 

indoxyl, 38. 

phosphoric acid, 45. 

sulphates, 46. 
Varieties of sugar, 56. 
Vaso-motor action, 10. 

Xanthine, 30, 100. 

Yellow-fever, 140. 



91. 



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